Presentation for students of the medical college "hypertension." Presentation on the topic "arterial hypertension" Arterial hypertension presentation

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HYPERTENSION DISEASE LECTURE PLAN: Definition of “Hypertension”, prevalence and relevance for a paramedic. 2. Etiology and pathogenesis of hypertension. 3. Clinical manifestations of the disease. 4. Classification of headaches. 5. Diagnosis of hypertension. 6. Complications of hypertension. 7. Hypertensive crises. 8. Principles of treatment. 9. Prevention of hypertension.

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RELEVANCE OF THE TOPIC STUDYED Hypertension is the most important cause of disability and premature mortality in the world. Hypertension is a risk factor in the development of atherosclerosis and ischemic heart disease (myocardial infarction). Hypertension is followed by atherosclerosis and myocardial infarction as a shadow behind a person. PROVEN!!! Regular measurement of blood pressure and keeping it normal reduces the development of myocardial infarction by 19-20%; the number of strokes by 43-45%

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In Russia, 42% of the population are diagnosed with hypertension (25% of the adult population; 50% of people over 60 years old) Russian hypertensive patients 34% do not know how to be treated correctly 12% know, but do not want to be treated 32% know, but are treated incorrectly 22% are treated Right

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RISK FACTORS NON-CORRECTABLE (IRREVERSIBLE) CORRECTABLE (REVERSIBLE) AGE AND GENDER men – over 55 years old women – over 65 years old HERITANCE SMOKING STRESS HYPODYNAMIA HIGH CHOLESTEROL DIABETES MELLITUS OBESITY EXCESSIVE SALT CONSUMPTION

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In medicine, the term “CHARACTER OF HYPERTENSION” has already firmly taken root - a person who likes to go to bed late - is exhausted to the limit at work - relieves stress with a cigarette or a large amount of alcohol - a lover of delicious food - a master of sorting things out mainly by shouting - always excited and trying to “break through the walls with his forehead” - afraid of being late somewhere and not being able to do something in time

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The main symptom of hypertension is increased blood pressure. Subjective sensations or complaints appear after damage to target organs. TARGET ORGANS HEART RETINA BRAIN KIDNEYS VESSELS

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HEART – left ventricular hypertrophy. Diagnostics: percussion enlargement of the borders of the heart, auscultation – deafness of the first tone, emphasis of the second tone on the aorta. Additional research methods: ECG, R-graphy of the chest organs, ultrasound of the heart. BRAIN – cerebrovascular accident (motor and sensory disorders, speech disorders, swallowing, consciousness, etc.) KIDNEYS – hypertensive nephropathy: hardening of the kidney vessels, leading to a decrease in the concentration function of the kidneys (nocturia, hypoisosthenuria), red blood cells, protein in the urine. Subsequently, chronic renal failure may develop (delay in the body of metabolic products, namely toxic substances that are excreted in the urine, uremia develops). For diagnosis: additional research methods (urinalysis, biochemical blood test, Zimnitsky test (polyuria oliguria anuria), nocturia, hypoisosthenuria. Biochemical blood test: increased urea, creatinine. RETINA - hypertensive retinopathy. Narrowing and tortuosity of the retinal arteries and dilation of the veins develop , hemorrhages in the fundus. Later, degeneration of the optic nerve develops in the form of white spots. All this can lead to complications such as retinal detachment and optic nerve atrophy with loss of vision - atherosclerosis.

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CLASSIFICATION OF ARTERIAL HYPERTENSION BY STAGE Stage I There are no objective signs of target organ damage Stage II At least one of the following manifestations of target organ damage is present: Left ventricular hypertrophy (according to X-ray, ECG or echocardiography); generalized or focal narrowing of retinal vessels; microalbuminuria, proteinuria and/or creatinymia 1.2-2.0 mg/dl; atherosclerotic changes (plaques) according to ultrasound examination or angiography (in the carotid arteries, aorta, iliac and femoral arteries). Stage III In addition to the listed signs of target organ damage, there are the following clinical manifestations. Heart: angina pectoris, myocardial infarction, heart failure. Brain: stroke, transient cerebrovascular accident. Hypertensive encephalopathy. Vascular dementia. Retina: hemorrhages or exudates with swelling (or without swelling) of the optic nerve. These signs are characteristic of malignant and rapidly progressing arterial hypertension. Kidneys: plasma creatinine more than 2 mg/dl. Kidney failure. Vessels: dissecting aortic aneurysm, occlusive lesions of arteries with clinical manifestations.

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Classification of hypertension by blood pressure level Category Blood pressure systolic (mm Hg) Blood pressure diastolic (mm Hg) Optimal< 120 < 80 Нормальное < 130 < 85 Высоко нормальное 130 - 139 85 - 89 ГИПЕРТЕНЗИЯ: Степень 1 140 - 159 90 - 99 Степень 2 160 - 179 100 - 109 Степень 3 >180 > 110 ISOLATED SYSTOLIC HYPERTENSION > 140< 90

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RISK STRATIFICATION BP LEVEL (mmHg) Other risk factors Grade 1 140–159 / 90-99 Grade 2 160-179 / 100-109 Grade 3 > 180 / > 110 COMPLICATION LEVEL I – no RF Low risk< 15% Средний риск 15 – 20% Высокий риск 20 – 30% II – 1 -2 ФР (кроме диабета) Средний риск 15 – 20% Средний риск 15 – 20% Очень высокий риск >30% III – 3 or more risk factors, or target organ involvement, or diabetes High risk 20 – 30% Moderate risk 15 – 20% Very high risk > 30% IV – clinical manifestations of diseases associated with blood pressure Very high risk > 30% Very high risk > 30% Very high risk > 30%

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COMPLICATIONS OF ARTERIAL HYPERTENSION Chronic heart failure Acute left ventricular failure Myocardial infarction Dissecting aortic aneurysm Angina pectoris Visual impairment Blindness Renal failure Stroke

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TREATMENT OF HYPERTENSION DISEASE Goal of therapy: The main goal of treatment is to achieve the target blood pressure level.< 140/90 мм.рт.ст. АД < 130/85 мм.рт.ст. (при сахарном диабете) АД < 125/75 мм.рт.ст. (при ХПН) Достижение целевого уровня АД должно быть постепенным и хорошо переноситься пациентом. Если пациент отнесен к высокому и очень высокому риску, то незамедлительно начинают медикаментозную терапию. При низком и среднем риске рекомендуется изменение образа жизни в течение 3-4 месяцев; при неэффективности начать медикаментозное лечение.

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Reduce elevated blood pressure levels to TARGET Increase quality of life, reduce changes in target organs The ultimate goal is to reduce the risk of complications

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DRUG THERAPY It is necessary to reduce blood pressure to the target gradually over 4-6 weeks, otherwise the quality of life deteriorates and complications from target organs arise (the brain suffers, blood circulation is impaired) Well treated: severe arterial hypertension, women, high level of education, high income , high level of culture, married. Poorly treated: smokers, alcoholics, repeated treatment, consuming a lot of salt.

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HYPOTENSIVE DRUGS Diuretics Hypothiazide, Veroshpiron ß - blockers Atenol, Concor Calcium antagonists Verapamil, Corinfar (Nifedipine) ACE inhibitors Enalapril, Capoten, Enap  adrenergic blockers Prazosin Angiotensin II receptor antagonists Losartan Centrally acting drugs Clonidine, Clonidine

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INDICATIONS FOR HOSPITALIZATION - Uncertainty of diagnosis and the need for special research methods to clarify the form of arterial hypertension - Difficulty in selecting drug therapy (frequent crises, resistance to therapy).

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INDICATIONS FOR EMERGENCY HOSPITALIZATION - Hypertensive crisis that is not relieved at the prehospital stage - Complications of arterial hypertension requiring intensive care and constant medical supervision (stroke, acute visual impairment, myocardial infarction, pulmonary edema, etc.)

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HYPERTENSION CRISIS (HC) is a pathological condition that manifests itself as a sharp deterioration in well-being against the background of increased blood pressure, is accompanied by the appearance or aggravation of existing cerebral and (or) cardiac symptoms and requires urgent treatment.

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ETIOLOGY OF HYPERTENSION CRISIS I. Diseases causing II. Endogenous Exogenous critical hypertensive provoking factors factors of the condition Primary (essential) arterial hypertension (AH) or essential hypertension (HD) Exacerbation of concomitant diseases (osteochondrosis, etc.) Stress and exercise Pheochromocytoma Excessive secretion of renin Salt abuse Diencephalic syndrome Acute or chronic ischemia brain Alcohol excess Acute and chronic glomerulonephritis Transient increase in secondary aldosteronism with sodium and water retention during the period of hormonal changes Meteorological changes Chronic pyelonephritis Termination of antihypertensive treatment Colds Influence of other drugs

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MAIN HAZARDS OF GK Local cerebral ischemia due to arteriolospasm Increased cerebral vascular permeability Increased intravascular pressure Increased risk of ischemic stroke Hypertensive encephalopathy Increased risk of vascular rupture (cerebral hemorrhages, aortic dissection, nasal and other bleeding) Increased afterload, increased myocardial consumption oxygen, activation of the reninangiotensin system Increased risk of cerebral edema Decreased renal blood flow (arteriolospasm) Increased risk of acute left ventricular failure, cardiac arrhythmias, myocardial ischemia (focal necrosis) Increased risk of developing renal failure

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IN THE PATHOGENESIS OF HA, THERE ARE: vascular mechanism - an increase in total peripheral resistance as a result of an increase in vasomotor (neurohumoral influence) and basal (with sodium retention) arteriolar tone; cardiac mechanism - an increase in cardiac output, myocardial contractility and ejection fraction in response to an increase in heart rate (HR) and circulating blood volume.

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CLASSIFICATION OF GK CLASSIFICATION I. A. N. Golikova II. M. S. Kushakovsky III. A. L. Myasnikov – N. A. Ratner IV. I. N. Bokareva Hyperkinetic Eukinetic Hypokinetic Neurovegetative Water-salt Convulsive (hypertensive encephalopathy) Type I (adrenal) Type II (noradrenal) uncomplicated complicated Cerebral Cardioischemic With acute left ventricular failure With dissecting aortic aneurysm With damage to eye structures With kidney damage

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CAUSES OF CRISES stress excessive physical activity abuse of alcohol and tobacco abrupt withdrawal of antihypertensive drugs inadequate therapy in women crises occur 6 times more often than in men

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COMPLAINTS OF PATIENTS WITH HA Cerebral Cardiac Symptoms of neurotic and autonomic dysfunction intense headache dizziness nausea, vomiting visual impairment, transient blindness, double vision, flashing “spots” before the eyes development of focal brain symptoms: numbness and/or decreased pain sensitivity of the tongue, lips, skin of the face and hands, a crawling sensation, the appearance of weakness in the limbs, transient hemiparesis (up to one day), short-term aphasia, convulsions, pain in the heart, palpitations, a feeling of interruptions, shortness of breath, chills, a feeling of fear, irritability, sweating, sometimes a feeling of heat, thirst at the end of the crisis - rapid, profuse urination with the release of light-colored urine

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TYPE I CRISIS (HYPERKINETIC) - acute rapid development of crisis - duration of minutes, hours (rarely up to a day) - complaints of headaches, palpitations, trembling throughout the body, increased sweating, cold extremities, dry mouth - upon examination - hand tremor, the skin has increased humidity, the extremities are cold to the touch - heart rate is 80 per minute, blood pressure is predominantly increased systolic, pulse pressure increases - at the end of the crisis there is copious urination - develops in the early stages of arterial hypertension - complications are not typical

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TYPE II CRISIS (HYPOKINETIC) - gradual development of crisis - duration of crisis is long (from several hours to several days) - complaints of severe headaches, heaviness in the head, nausea, vomiting, transient visual disturbances, noise, ringing in the ears, compressive pain in the region of the heart, drowsiness, lethargy - disorientation, confusion - heart rate 60-80 per minute, blood pressure is dominated by a rise in diastolic pressure, pulse pressure decreases - in the later stages of arterial hypertension develops against the background of initial high blood pressure - possible complications: stroke, myocardial infarction, angina pectoris , cardiac asthma, etc.

Arterial hypertension is a stable increase in systolic blood pressure up to 140 mmHg. and above and/or diastolic arterial pressure up to 90 mm Hg. and higher, based on 2 or more consecutive patient visits with an interval of at least 1 week.

CLASSIFICATION OF ARTERIAL HYPERTENSION Arterial hypertension Primary hypertension (essential hypertension, or essential hypertension) is a chronic disease of unknown etiology with a hereditary predisposition, resulting in the interaction of genetic factors - the external environment, characterized by a stable - increase in blood pressure. Secondary hypertension (symptomatic) is based on one specific cause, the elimination of which is important not only for reducing or normalizing blood pressure, but also for preventing complications.

ETIOLOGY Essential hypertension ETIOLOGY Essential hypertension Genetic predisposition Approximately 50% of patients have a hereditary predisposition to EG caused by a mutation in the genes [mutation of angiotensinogen, angiotensin II receptors, angiotensin-converting enzyme, renin, aldosterone synthetase, β-subunit of sodium-sensitive amiloride channels of the renal epithelium and other sodium

Other factors Obesity increases the risk of hypertension fivefold. More than 85% of cases of hypertension occur in patients with a body mass index of more than 25. body mass index Smoking: reduces endothelium-dependent vasodilation, increases the activity of the sympathetic nervous system, is a risk factor for the development of coronary heart disease. sympathetic nervous system of coronary heart disease Excessive consumption table salt: excess sodium increases the volume of circulating blood, causes swelling of the walls of the carterioles, increases the sensitivity of the vascular wall to vasoconstrictor factors. Carterioles Insufficient intake of calcium and magnesium, trace elements and vitamins from water and food. Alcohol abuse. Low physical activity, lack of exercise. Psycho-emotional stressful situations.

The appearance of cardial hypertension depends on the person’s age. At a young age, mainly secondary hypertension due to smoking, alcoholism, drugs, vertebrobasilar insufficiency, congenital anomalies of blood vessels, kidneys, adrenal glands, pituitary gland. In middle age due to excess body weight, neuropsychic stress or previous diseases with damage to the heart, blood vessels, and kidneys. And after the age of 40, this is almost always the result of sclerotic vascular lesions. Gestational hypertension is hypertension that develops in some women during pregnancy. It usually resolves after childbirth, but sometimes the disease can be prolonged, and women who have had hypertension in pregnancy, as well as preeclampsia and eclampsia, also accompanied by cardial hypertension, are more likely to develop hypertension in subsequent years. preeclampsia-eclampsia In Africans living in an industrial society, essential hypertension occurs four times more often than in whites, develops more quickly and leads to greater mortality, the prevalence, but not the severity, of essential hypertension in them decreases with a decrease in overt or hidden racism

CLASSIFICATION CLASSIFICATION (by degree) OF ARTERIAL HYPERTENSION BEYOND BP LEVEL (according to WHO and MLG experts, 1999) BP category SBP, mmHg DBP, mmHg Optimal

By stage Stage I hypertension assumes the absence of changes in target organs. Stage II hypertension is characterized by the presence of one or more changes in target organs. Stage III hypertension is established in the presence of one or more associated (concomitant) conditions.

55 years old women > 65 years old Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus" title=" Risk factors used for risk stratification Value of systolic and diastolic blood pressure (grade 1-3) Age men > 55 years old women > 65 years old Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus" class="link_thumb"> 12 !} Risk factors used for risk stratification Value of systolic and diastolic blood pressure (grade 1-3) Age men > 55 years women > 65 years Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus Family cases of early development of hypertension, cardiovascular diseases 55 years old women > 65 years old Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus > 55 years old women > 65 years old Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus Family cases early development of hypertension, cardiovascular diseases"> 55 years old women > 65 years old Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus" title=" Risk factors used for risk stratification Value of systolic and diastolic blood pressure (grade 1-3) Age men > 55 years women > 65 years Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus"> title="Risk factors Used for risk stratification Value of systolic and diastolic blood pressure (grade 1-3) Age men > 55 years women > 65 years Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus"> !}

Other factors, Smoking Excessive consumption of table salt Insufficient intake of calcium and magnesium, trace elements and vitamins from water and food. calcium magnesium Alcohol abuse. Low physical activity, physical inactivity. physical inactivity. Psycho-emotional stressful situations. Reduced HDL cholesterol Increased LDL cholesterol Microalbuminuria (mg/day) in diabetes Impaired glucose tolerance Increased fibrinogen in the blood High-risk socioeconomic groups

300 mg/day) and/or a slight increase in plasma creatinine concentration (1.2 2 mg/dL) or microalbuminuria ProteSign" title=" Target organ damage Left ventricular hypertrophy Left ventricular hypertrophy Proteinuria (>300 mg/ day) and/or a slight increase in plasma creatinine concentration (1.2 2 mg/dl) or microalbuminuria ProteSign" class="link_thumb"> 14 !} Target organ damage Left ventricular hypertrophy Left ventricular hypertrophy Proteinuria (>300 mg/day) and/or a slight increase in plasma creatinine concentration (1.2-2 mg/dl) or microalbuminuria ProteSigns of atherosclerotic lesions of the carotid, iliac and femoral arteries, atherosclerotic aorta Generalized or focal narrowing of the retinal arteries 300 mg/day) and/or a slight increase in plasma creatinine concentration (1.2 2 mg/dl) or microalbuminuria ProteSign "> 300 mg/day) and/or a slight increase in plasma creatinine concentration (1.2 2 mg/dl) dl) or microalbuminuria ProteSigns of atherosclerotic lesions of the carotid, iliac and femoral arteries, atherosclerotic aorta Generalized or focal narrowing of the retinal arteries "> 300 mg/day) and/or a slight increase in plasma creatinine concentration (1.2 2 mg/dl) or microalbuminuria ProteSign" title="Target organ damage Left ventricular hypertrophyLeft ventricular hypertrophy Proteinuria (>300 mg/day) and/or a slight increase in plasma creatinine concentration (1.2 2 mg/dl) or microalbuminuria ProteSign"> title="Target organ damage Left ventricular hypertrophy Left ventricular hypertrophy Proteinuria (>300 mg/day) and/or a slight increase in plasma creatinine concentration (1.2 2 mg/dl) or microalbuminuria Proteinuria creatininemicroalbuminuria Sign"> !}

Associated clinical conditions Ischemic stroke Hemorrhagic stroke Transient cerebrovascular accident Myocardial infarction Angina pectoris Coronary revascularization Congestive heart failure Heart failure Diabetic nephropathy Renal failure (plasma creatinine above 2 mg/dl) Dissecting aneurysm Severe hypertensive retinopathy Hemorrhage or exudation ata Hemorrhages exudates Swelling of the optic nipple nerve

Pathogenesis of Essential AH OUWOWWOWWOWW PRESORNAYDOMINANT A! A! Subcortical structures A! pressor centers of the medulla oblongata and hypothalamic nuclei A! Sympathoadrenal s-we A! humoral pressor systems: ADH, synthesis of releasing factors ACTH, TSH Distribution of the peripheral sump. Spasm through the sympathoadrenal system Renal ischemia A! YUGA and A! RAAS Increased. General peripheral resistance to blood flow (sympathy of ADH, ACTH) A! SAS and RAAS Reomodeling of the vessel. Walls AFTER LIQUIDATION AD-not N

CAUSES OF SYMPTOMATIC ARTERIAL HYPERTENSION 1) kidney disease: parenchyma (glomerulonephritis, chronic pyelonephritis, diabetic nephropathy, amyloidosis, hydronephrosis, nephrosclerosis); vascular system (atherosclerosis, vasculitis, endarteritis, thrombosis, embolism, renal aneurysm, venous stenosis and thrombosis, renal vascular injury); anomalies of the kidneys and urinary system (polycystic disease, hypoplasia); - secondary kidney damage due to tuberculosis, diffuse diseases of the connected tissue (SLE, systemic scleroderma); 2) endocrine hypertension (pheochromocytoma; primary hyperaldosteronism (Conn syndrome); Cushing's disease (syndrome); hyperparathyroidism; acromegaly; menopausal hypertension; 3) hemodynamic hypertension (aortic atherosclerosis; stenosis of the carotid and vertebrobasilar arteries; coarctation of the aorta; aortic insufficiency; rheological hypertension ( true polycythemia); 4) neurogenic hypertension (vascular diseases and brain tumors; inflammatory diseases - encephalitis, meningitis, poliomyelitis; brain injury; polyneuritis. 5) special forms of medicinal symptomatic hypertension (anabolic steroids and mineralocorticoids, oral contraceptives containing progesterone and estrogens, sympathomimetics, indomethacin and others).

Renal arterial hypertension Renovascular arterial hypertension Renovascular (vasorenal) hypertension (RVAH) is a persistent increase in arterial pressure caused by circulatory disorders of one or both kidneys as a result of insufficient blood supply. CAUSES Congenital: -fibromuscular dysplasia of the kidney carteries; - developmental anomalies of the aorta; - compression of the renal carteria Acquired: - atherosclerotic process; -thrombosis; - embolism of the renal cartery; -pancarteritis; --nephroptosis

RENAL ISCHEMIA A! YUGA A!RENIN release+ A! RASS formation of ANGIOTENSIN II Stimulation of the zona glomerulosa of the adrenal cortex Release of ALDOSTERONE Na retention Delay of H2O in dist. parts of the nephron BP Secretion of ADH + delay of H2O bcc Powerful vasoconstrictor BPSS Acts on the HYPOTHALAMUS and enhances the consumption of H2O + stimulation of the “Thirst Center”

Clinical picture - Acute onset of the disease, characterized by a sharp increase in blood pressure in men over 50 years of age or in women under 30 years of age. - From the very beginning of the disease, high blood pressure levels are observed that are resistant to therapy. - As a rule, there are no hypertensive crises. - Predominant increase in DBP, pulse blood pressure is reduced. - Tendency to orthostatic hypotension. - Vascular systolic murmur or systolic-diastolic murmur in the peri-umbilical region (in the projection of the renal cartery arising from the aorta). - Transient or persistent signs of renal dysfunction.

Renoprival carterial hypertension Damage to the renal glomeruli Damage to the renal parenchyma: glomerulonephritis, systemic scleroderma, SLE, Amyloidosis Diabetic nephropathy IMPAIRMENT OF VASODILATORY SUBSTANCES BY THE KIDNEY: Bradykinin Prostaglandins Impaired ability of the kidneys to inactivate vasopressor substances When the glomeruli are damaged, fluid secretion is impaired - increase BCC - increase in blood pressure

GLOMERULONEPHRITIS CLINIC - Young age. - Predominant increase in DBP, with SBP not exceeding 180 mm Hg. - Blood pressure stability. - No crises. The presence of at least minimal changes in urine examination, with a predominance of red blood cells and casts. The diagnosis is established on the basis of Doppler studies and x-ray methods, but the final diagnosis is made only on the basis of a biopsy.

Chronic pyelonephritis In this case, clinical signs of the underlying disease are determined: chilling, dysuria, oliguria, puffiness of the face, low-grade fever, signs of inflammation in the blood and urine. But with a long history, hypertension becomes persistent, with a predominant increase in DBP. When examining urine against the background of exacerbation of pyelonephritis, persistent hypoisosthenuria, leukocyturia and bacteriuria are determined, and sometimes hematuria. Urine culture is required. A blood test reveals clinical signs of inflammation, and there may be anemia. The diagnosis is established on the basis of instrumental research methods - identifying deformation of the collecting apparatus, reducing the size of the kidneys and dysfunction, asymmetry of the lesion.

Polycystic Increased blood pressure in polycystic disease is the result of ischemia of the parenchyma due to cystic degeneration, nephrosclerosis and/or the addition of a secondary infection and secondary pyelonephritis. With significant enlargement of the kidneys, the diagnosis can be suspected by palpation, and confirmed using instrumental research methods (urography, ultrasound, computed tomography).

Endocrine The development of Cushing's syndrome is associated with a cortisol-secreting tumor (adenoma or adenocarcinoma) of one of the adrenal glands or long-term treatment with glucocorticoids. The pathogenesis of hypertension in this form of secondary hypertension has not been fully established. It is assumed that the increase in blood pressure is caused by: 1) hyperproduction of cortisol with activation of the central nervous system, 2) increased sensitivity of blood vessels to the vasoconstrictor effect of norepinephrine and other vasopressor agents, 3) retention of sodium and water by the kidneys with an increase in central nervous system, since hypercotrizolemia is usually combined with excess formation of mineralocorticoids, 4) excessive formation of angiotensin II.

Arterial hypertension with hypercortisolism, as a rule, does not reach high numbers, is systolic-diastolic in nature, occurs without crises and has a relatively benign course. But if detected untimely and untreated, it can lead to vascular complications and death.

Hyperaldosteronism Hormone-producing tumor of the zona glomerulosa of the adrenal cortex. The level of Na ions in the blood and the wall of blood vessels of the bcc increases the sensitivity of the brain to catecholamines; HYPERTHYROIDOSIS - OPSS; Heart rate; UO HYPOTERIOSIS - myxedema - accumulation of acidic glycosaminoglycans - which are sorbents of Na H2O + comp. The tissue surrounding the neurovascular bundles compresses the peripheral vascular resistance + blood pressure and edema occurs

Hemodynamic carterial hypertension Hemodynamic carterial hypertension is associated with damage to the heart and blood vessels and is distributed as follows: a) systolic hypertension in atherosclerosis, aortic regurgitation; b) regional hypertension with coarctation of the aorta; c) hyperkinetic hypertension in carteriovenous fistulas. Arterial hypertension as a result of atherosclerosis of the aorta is diagnosed on the basis of the following signs: advanced age of the patient, accent of the second heart sound and a metallic tint over the aorta, systolic murmur over the aorta, increased systolic blood pressure, signs of atherosclerosis of the peripheral arteries, dilatation of the aorta according to X-ray and ultrasound examinations.

Hemodynamic carterial hypertension Arterial hypertension during aortic regurgitation is characterized by an increase in systolic and a decrease in diastolic blood pressure with a high level of pulse pressure. Arterial hypertension with coarctation of the aorta is manifested by an increase in blood pressure in the upper extremities and a decrease in blood pressure in the lower extremities. On palpation, intense pulsation of the intercostal arteries is determined, a decrease in the pulsation of peripheral arteries in the lower extremities; on auscultation, a rough systolic murmur is detected above the projection of the thoracic aorta along the anterior surface of the thoracic

Clinic of cardial hypertension PATIENT'S COMPLAINTS: pain in the heart, stop. after taking sedatives. palpitations, headache. dizziness, tinnitus, neurological disorders - emotional lability, irritability, visual impairment. In the presence of heart failure - attacks of suffocation.

OBJECTIVE EXAMINATION The general condition of the patient is satisfactory. As the disease progresses and complications appear, the patient's general condition can range from moderate to severe (hypertensive crisis, acute and chronic heart failure, transient ischemic attacks). Skin color - hyperemia. Body weight: More often than not, patients are overweight or obese.

Diagnostic program of mandatory studies when identifying hypertension Mandatory studies: - collection of complaints and anamnesis; - clinical examination; - measuring blood pressure in both arms; - measurement of blood pressure in the lower extremities - measurement of body weight and waist circumference; - laboratory examination: general blood and urine tests, urine analysis according to Nechiporenkoy, creatinine, cholesterol, triglycerides, glucose, potassium, blood sodium); - ECG in 12 standard leads; - echocardiography; - examination of the fundus. Additional studies: - determination of microalbuminuria; - daily monitoring of blood pressure; - ultrasound examination of the kidneys; - rheoencephalography; - daily proteinuria; - with a decrease in the relative density of urine - urine analysis according to Zimnitsky.

Laboratory research methods: Clinical blood test without changes. Clinical urine analysis does not detect changes in the initial stages of the disease. With the development of hypertensive nephropathy, microalbuminuria is determined, and later proteinuria. Microscopy of urine sediment: leukocytes, micro- and macrohematuria, granular casts. Biochemical blood test: hypercholesterolemia, hypertriglyceridemia, reduction in high-density cholesterol. X-ray examination reveals left ventricular hypertrophy, atherosclerotic lesions of the aorta, and venous congestion in the lungs. Electrocardiography: a sign of left ventricular hypertrophy, systolic overload of the left ventricle, a sign of coronary insufficiency, a negative or biphasic T wave, depression of the S-T segment, a sign of previous myocardial infarction, cardiac rhythm and conduction disturbances. Echocardiography: thickening of the interventricular septum, the posterior wall of the left ventricle, increased myocardial mass and cardiac voids, decreased myocardial contractility according to ejection fraction indicators. When performing Doppler echosonography, atherosclerotic lesions of the carotid arteries are detected. Examination of the fundus of the eye determines angiopathy of the retina, mainly of the capillaries, but damage to larger vessels - the carteries - is possible. At the same time, pathological changes occur in the venous vessels.

Electrocardiography for hypertension 1. systolic overload of the left ventricle, 2. sign of left ventricular hypertrophy, 3. sign of coronary insufficiency, 4. negative or biphasic T wave, 5. depression of the S-T segment, 6. sign of previous myocardial infarction, 7. rhythm and conduction disturbances hearts.

How to treat hypertension? Therapy is aimed at solving the following problems: Achieving the target blood pressure level. It should be no more than 140/90. For elderly patients with severe hypertension, a reduction in systolic pressure to 160 mmHg is recommended. Art. Correction of modifiable risk factors. Prevention and treatment of associated pathologies. One of the main therapeutic options is lifestyle modification.

Loss of body weight. A decrease in weight for every 10 kg can reduce blood pressure by up to 20 mmHg. Art. Limiting table salt consumption (recommended no more than 5 g per day). It has been found that in cultures with a traditionally high salt intake, the incidence of the disease is higher. Taking 25 g of salt per day increases the risk of hypertension by 3 times. Dynamic loads reduce pressure by 4 mm Hg. Art. Half-hour classes 4 times a week are enough. Quitting alcohol. It is allowed to consume up to 30 g of alcohol per day for men and up to 15 g for women. This measure will further reduce the pressure by 2–4 mmHg. Art. Diet therapy. It is recommended to increase the consumption of foods rich in dietary fiber, potassium, calcium, and magnesium. You need to reduce your fat intake. The effectiveness of the product reduces blood pressure by 8–14 mmHg. Art. Increasing resistance to psycho-emotional stress (mastering techniques of psychological self-regulation).

Main groups of drugs Diuretics Diuretics To combat hypertension with preserved renal function, low doses of thiazide and thiazide-like diuretics (indapamide, hydrochlorothiazide, chlorthalidone) are prescribed. In recent years, preference has been given to indapamide, since, in comparison with other diuretics, it has an additional vasodilating effect and has virtually no effect on metabolic processes. Diuretics can be used as monotherapy or in combination with other antihypertensive agents. A feature of modern diuretics is to reduce the risk of addiction. Thiazide-like diuretics are the drugs of choice for heart failure in older age groups, as well as in patients with osteoporosis and coronary artery disease. Furosemide and other loop diuretics are not used for the treatment of hypertension due to their low antihypertensive effectiveness and high incidence of side effects. The use of this group becomes necessary only when there is a marked decrease in the function of the heart and kidneys in the treatment of hypertension

Calcium antagonists representatives of this group are derivatives of nifedipine, verapamil and diltiazem. Until quite recently, taking “nifedipine 10 mg sublingually” was the standard of care for emergency care during a hypertensive crisis. Now this method of reducing pressure is used much less frequently. Modern relatives of nifedipine (amlodipine, felodipine, lacidipine, prolonged forms of nifedipine, etc.) are used once a day and are characterized by fewer side effects. Calcium antagonists are especially useful in the combination of hypertension with peripheral vascular atherosclerosis, stable and vasospastic angina; they can also be prescribed for the treatment of hypertension in pregnant women. This group cannot be used directly after myocardial infarction and in patients suffering from heart failure. Verapamil and diltiazem, in addition to their effect on blood pressure, have been successfully used to treat angina pectoris and arrhythmias

ACE inhibitors A group that includes medications for hypertension such as ienalapril, captopril, perindopril, ramipril, lisinopril. A feature of ACE inhibitors is their ability, in addition to lowering blood pressure, not only to prevent, but also to correct the negative consequences of its long-term existence. It is known that about 18% of patients with hypertension die from renal failure, and in this situation it is ACE inhibitors that help reduce the negative impact of hypertension in patients predisposed to diabetes mellitus and kidney pathology. In addition, the group may be useful for a significant number of patients with underlying kidney disease who develop symptomatic hypertension. Medicines for hypertension from the group of ACE inhibitors suppress the formation of the hormone angiotensin II, the activity of which is especially high when the kidneys are damaged, thereby preventing their damage. In addition, ACE inhibitors actively inhibit pathological changes caused by the same angiotensin II in the heart and blood vessels. ACE inhibitors are especially indicated in cases of heart failure accompanying high blood pressure, asymptomatic left ventricular dysfunction, diabetes mellitus, previous myocardial infarction, non-diabetic nephropathy, microalbuminuria and metabolic syndrome

Sartans (angiotensin receptor blockers) Sartans, related to the group of ACE inhibitors, have similar mechanisms of action. But unlike ACE inhibitors, sartans are better tolerated by patients with hypertension - they are less likely to cause side effects. In addition, the most important features of angiotensin II receptor blockers include the ability of these drugs to protect the brain from the effects of hypertension, including restoring it after a stroke. Sartans also improve renal function in diabetic nephropathy, reduce left ventricular hypertrophy, and improve heart function in patients with heart failure. Losartan, valsartan, irbesartan, candesartan, telmisartan are prescribed for similar indications, but when ACE inhibitors are poorly tolerated

Beta-blockers This group is another important group of drugs for hypertension, it includes atenolol, bisoprolol, metoprolol, nebivolol, etc. Along with diuretics, they are still drugs of primary importance for the treatment of hypertension. The prescription of beta blockers is especially appropriate when hypertension is combined with coronary artery disease, heart failure, thyroid hyperfunction, arrhythmias and glaucoma. This is also one of the few antihypertensive groups that is approved for use in pregnant women. On the other hand, the use of beta blockers is impossible in some groups of patients due to serious side effects

Alpha-blockers (prazosin, terazosin, doxazosin, tamsulosin, alfuzosin) are widely used in urology and are often prescribed in combination with first-line drugs for the combination of hypertension and prostate hypertrophy. In cardiology, alpha-blockers are used for the treatment of Prinzmetal's angina (prazosin) and the symptomatic treatment of secondary hypertension (pheochromocytoma, clonidine withdrawal syndrome, hypertensive crises while taking MAO inhibitors). Alpha blockers are the only class of antihypertensive drugs that improve the lipid profile. However, they often cause first-dose hypotension and orthostatic hypotension, which the doctor usually warns the patient about. To achieve target blood pressure values, it is rational to combine drugs in this group with ACE inhibitors and calcium channel blockers. ACE inhibitors

Centrally acting drugs are still quite widely used for the treatment of hypertension, but their place is limited to use in combination therapy, the treatment of hypertensive crises and for the treatment of hypertension in pregnant women. The first generation of centrally acting drugs include methyldopa (Dopegit), guanfacine (Estulik) and clonidine (Clonidine), the second generation includes rilmenidine (Albarel) and moxonidine (Physiotens). Clonidine is the drug of choice for uncomplicated hypertensive crises. Methyldopa is the drug of choice for the treatment of hypertension in pregnant women. Compared to its predecessors, the second generation of centrally acting drugs is better tolerated. Currently, moxonidine is especially recommended for use in overweight patients, but always in combination with first-line drugs. To achieve target blood pressure levels, it is rational to combine alpha-blockers with diuretics, ACE inhibitors and calcium antagonists. Hypertension in pregnant women The new drug Aliskiren (Rasilez), a direct inhibitor of renin and prorenin, also belongs to this group. It has been shown to effectively lower blood pressure and reduce proteinuria, but so far its positive effect on cardiovascular morbidity and mortality has not been proven due to its relatively short lifespan. Several studies are currently being conducted on this drug. Direct vasodilators (hydralazine, minoxidil) are currently used extremely rarely.

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Definition

Arterial hypertension is a stable increase in blood pressure - systolic to a level of 140 mm Hg and above and/or diastolic to a level of 90 mm Hg. Art and higher according to at least two measurements using the Korotkoff method at two or more consecutive patient visits with an interval of at least 1 week.

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Classification

There are essential (primary) and secondary arterial hypertension. Essential arterial hypertension accounts for 90-92%, secondary hypertension accounts for about 8-10% of all cases of high blood pressure.

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Essential arterial hypertension

a chronic disease of unknown etiology with a hereditary predisposition, resulting from the interaction of genetic and environmental factors, characterized by a stable increase in blood pressure in the absence of damage to its regulating organs and systems.

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Classification of blood pressure levels and degrees of arterial hypertension (WHO/MOAG, 1999)

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Notes

If systolic and diastolic blood pressure levels fall into different classification categories, then the higher category must be selected. As a criterion for diagnosing hypertension, the levels of systolic and diastolic blood pressure should be used equally; to determine the degree of isolated systolic hypertension, the gradations given in the column “systolic blood pressure” are used.

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Risk stratification of cardiovascular complications

Experts from the WHO and IAHA have proposed risk stratification into four categories (low, medium, high and very high) or risk 1, 2, 3, 4. The risk in each category is calculated based on an average of 10 years of data on the probability of death from cardiovascular diseases diseases, as well as from myocardial infarction and stroke. To determine the individual risk level for a given patient for developing cardiovascular complications, it is necessary to assess not only the degree of hypertension, but also the number of risk factors, the degree of target organ damage and the presence of concomitant cardiovascular diseases.

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Factors influencing prognosis and used for risk stratification

Risk factors for cardiovascular diseases 1. Used for risk stratification Value of systolic and diastolic blood pressure Age: men over 55 years old women over 65 years old Smoking Total blood cholesterol level more than 6.5 mmol/l Diabetes mellitus Family cases of early development of cardiovascular diseases

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2. Other factors adversely affecting the prognosis Reduced levels of HDL cholesterol Increased levels of LDL cholesterol Microalbuminuria (30-300 mg/day) in diabetes Impaired glucose tolerance Obesity Sedentary lifestyle Increased levels of fibrinogen in the blood Socio-economic groups at increased risk

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Target organ damage Left ventricle hypertrophy (ECG, Echo-CG, Rtg) Proteinuria and/or slight increase in plasma creatinine concentration Ultrasound or radiological signs of atherosclerotic lesions of the carotid, iliac and femoral arteries, aorta Generalized or focal narrowing of the retinal arteries

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Associated clinical conditions Cerebrovascular diseases: Ischemic stroke Hemorrhagic stroke Transient ischemic attacks Cardiac disease: MI Angina Coronary revascularization Congestive heart failure Kidney disease: Diabetic nephropathy Renal failure Vascular disease: Dissecting aneurysm Peripheral arterial disease with clinical manifestations Severe hypertensive retinopathy Hemorrhages: swelling or exudates Nipple swelling optic nerve

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Risk stratification for assessing the prognosis of patients with hypertension

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Risk levels (risk of stroke or myocardial infarction) in the next 10 years:

Low risk (risk 1) – less than 15% Medium risk (risk 2) – 15-20% High risk (risk 3) – 20-30% Very high risk (risk 4) – 30% and above

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Low risk group (risk 1). This group includes men and women under 55 years of age with hypertension in the absence of other risk factors, target organ damage, and associated cardiovascular disease. Medium risk group (risk 2). This group includes patients with grade 1 or 2 hypertension. The main sign of belonging to this group is the presence of 1-2 other risk factors in the absence of target organ damage and associated cardiovascular diseases.

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High risk group (risk 3). This group includes patients with grade 1 or 2 hypertension, 3 or more other risk factors or target organ damage or diabetes. The same group includes patients with stage 3 hypertension without other risk factors, without target organ damage, without concomitant cardiovascular diseases and diabetes. Very high risk group (risk 4). This group includes patients with any degree of hypertension with concomitant cardiovascular diseases, as well as with stage 3 hypertension with the presence of other risk factors and/or target organ damage and/or diabetes, even in the absence of concomitant diseases.

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Classification of secondary hypertension

Secondary systolic-diastolic hypertension 1. Renal 1.1 Diseases of the renal parenchyma Acute and chronic glomerulonephritis Hereditary nephritis Chronic pyelonephritis Interstitial nephritis Polycystic kidneys Kidney damage in systemic connective tissue diseases and systemic vasculitis Diabetic nephropathy Hydronephrosis Renal tuberculosis Congenital renal hypoplasia Mi Fragile nephropathy Goodpasture's syndrome

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1.2 Renovascular hypertension Atherosclerosis of the renal arteries Fibromuscular hyperplasia of the renal arteries Thrombosis of the renal arteries and veins Aneurysms of the renal arteries Nonspecific aortoarteritis 1.3 Renin-producing kidney tumors 1.4 Primary renal sodium retention (Liddle syndrome) 1.5 Nephroptosis

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2. Endocrine Adrenal (Itsenko-Cushing’s syndrome, congenital virilizing adrenal hyperplasia, primary hyperaldosteronism, pheochromocytoma) Hypothyroidism Acromegaly Hyperparathyroidism Carcinoid 3. Coarctation of the aorta 4. Hypertension during pregnancy

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5. Neurological disorders Increased intracranial pressure (brain tumor, encephalitis, respiratory acidosis) Quadriplegia Lead intoxication Acute porphyria Hypothalmic (diencephalic) syndrome Familial dysautonomia Guillain-Barré syndrome Sleep apnea of ​​central origin

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6. Acute stress, including postoperative Psychogenic hyperventilation Hypoglycemia Burn disease Pancreatitis Withdrawal symptoms in alcoholism Crisis in sickle cell anemia Condition after resuscitation measures

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7. Hypertension induced by drugs, as well as with exogenous intoxications Taking oral contraceptives Treatment with corticosteroids, mineralocorticoids, sympathomimetics, estrogens Treatment with monoamine oxidase inhibitors simultaneously with the intake of foods rich in tyramine Intoxication with lead, thallium, cadmium 8. Increase in BCC Excessive intravenous infusions Polycythemia vera 9. Alcohol abuse (chronic alcoholism)

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Systolic hypertension

1. Increased cardiac output Aortic valve insufficiency Arteriovenous fistula, open aortic duct S-m thyrotoxicosis Paget's disease Hypovitaminosis B Hyperkinetic type of hemodynamics 2. Sclerotic rigid aorta

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Examples of diagnosis formulation

Arterial hypertension 1st degree. Risk 2. Dyslipidemia. AG 2 tbsp. Risk 3. Hypertensive heart H1. Ventricular extrasystole. AG 2 tbsp. Risk 4. Diabetes, type 2, stage of clinical-metabolic subcompensation, middle stage. severity, diabetic microangiopathy of the vessels of the lower extremities. AG 3 tbsp. Risk 4. IHD: angina pectoris FC 2. Atherosclerosis of the aorta, coronary arteries. H 1. Polycystic kidney disease. Chr. pyelonephritis, without exacerbation. Secondary nephrogenic hypertension.

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General tactics for managing people with hypertension

After establishing a diagnosis of hypertension and assessing cardiovascular risk, individual patient management tactics are developed. Important aspects of managing a patient with hypertension are: Motivating the patient for treatment and compliance with recommendations for lifestyle changes and drug therapy. The experience and knowledge of the doctor and the patient’s trust in him. Decision on the appropriateness and choice of drug therapy.

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Diagnostics

Taking an anamnesis to determine the duration of the increase in blood pressure, its levels, the presence of hypertensive crises; factors provoking increases in blood pressure; clarify the presence of signs that allow one to suspect the secondary nature of hypertension: family history of renal diseases; a history of kidney disease, bladder disease, hematuria, abuse of analgesics; use of various medications or substances: OK, GSK, NSAIDs, erythropoietin, cyclosporine; long-term work with lead salts; a history of endocrine diseases; paroxysmal episodes of sweating, anxiety headaches, palpitations (pheochromocytoma); muscle weakness, paresthesia, cramps (aldosteronism)

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identify factors aggravating the course of hypertension: the presence of dyslipidemia, diabetes, other heart and vascular diseases; aggravated medical history of hypertension, diabetes, and other CVDs in close relatives; smoking; nutritional features; level of physical activity; alcohol abuse; snoring, sleep apnea; personal characteristics of the patient.

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carefully identify the patient’s complaints indicating damage to target organs: brain, eyes - presence and nature of headache, dizziness, sensory and motor disorders, blurred vision; heart – pain in the chest, their connection with increases in blood pressure, emotional and physical stress, palpitations, interruptions in heart function, shortness of breath; kidneys – thirst, polyuria, hematuria, nocturia; peripheral arteries – coldness of the extremities, intermittent claudication. assess the possible influence of environmental factors, marital status, and nature of work on hypertension; clarify medical, social and work history.

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Physical examination

During a physical examination, the physician should identify POM and signs of secondary hypertension. Be sure to measure the patient’s height, weight, waist circumference, and calculate BMI. The secondary nature of hypertension may be indicated by the following data revealed during the examination: Symptoms of the disease or Itsenko-Cushing syndrome; Neurofibromatosis of the skin (sm pheochromocytoma); Kidney enlargement (polycystic disease, space-occupying formations); Weakened or delayed pulse in the femoral artery and reduced blood pressure on it (coarctation of the aorta, nonspecific aortoarteritis); Rough systolic murmur above the aorta, in the interscapular region (coarctation of the aorta, aortic diseases); Auscultation of the abdominal area - noises over the area of ​​the abdominal aorta, renal arteries (renal artery stenosis - vasorenal hypertension).

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POM should be suspected in the following cases: brain – auscultation of murmurs over the carotid arteries, motor and sensory disorders; retina of the eye – changes in the vessels of the fundus; heart – increased apical impulse, rhythm disturbances, presence of symptoms of CHF (wheezing in the lungs, presence of peripheral edema, enlarged liver); peripheral arteries – absence, weakening or asymmetry of the pulse, coldness of the extremities, symptoms of skin ischemia; carotid arteries - systolic murmur over the area of ​​the arteries.

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Standard laboratory tests

Fasting plasma glycemia Glucose tolerance test General CL LDL CL HDL TG TG Potassium Uric acid Creatinine Estimated creatinine clearance or glomerular filtration rate Hemoglobin and hematocrit Urinalysis (with determination of microalbuminuria); quantitative analysis of proteinuria.

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Standard instrumental studies

ECG Echo-CG Ultrasound of the carotid arteries Fundus examination Home blood pressure measurement 24-hour blood pressure monitoring Measurement of pulse wave velocity

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Special research methods

To confirm secondary hypertension, the following studies are carried out: determination of the concentration of renin, aldosterone, corticosteroids, catecholamines in plasma and/or urine, angiography, ultrasound of the kidneys and adrenal glands, CT, MRI of the relevant organs, kidney biopsy.

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Lifestyle interventions

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General principles of drug treatment of patients with hypertension

Antihypertensive therapy should be continuous; At the beginning of treatment, monotherapy is prescribed; If the effect of the drug is insufficient, its dosage is increased or a second drug is added; It is advisable to use long-acting drugs to achieve a 24-hour effect with a single dose.

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Choice of antihypertensive drugs

The effectiveness of antihypertensive therapy is assessed by the level of blood pressure reduction. As both initial and maintenance therapy, drugs of 5 main groups can be used: thiazide and thiazide-like diuretics, calcium channel blockers, ACE inhibitors, angiotensin 2 receptor blockers and beta blockers. Drugs of these classes can be used both as monotherapy and low-dose fixed combinations.

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Indications and contraindications for prescribing the main groups of antihypertensive drugs

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Preferred antihypertensive drugs for target organ damage and associated clinical diseases

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Therapy selection strategy (monotherapy/combination therapy)

Regardless of the choice of drugs, the use of monotherapy achieves the desired level only in a limited number of patients. To achieve the target blood pressure level, most patients require the use of more than one antihypertensive drug. Initial therapy can be carried out using either monotherapy or the combined use of two drugs in low doses, followed by increasing the dose or number of drugs if necessary. The use of monotherapy as initial therapy is possible with a slight increase in blood pressure, with a low and moderate risk of developing CVD complications. Preference should be given to the combined use of two drugs in low doses in cases where the initial blood pressure level corresponds to grade 2 or 3 hypertension or the overall risk of complications is high.

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Fixed-dose combinations of drugs are preferred because simplifying treatment has a better chance of adherence to therapy. A reduction in the risk of complications is observed with the following combinations: diuretic + ACE inhibitor or angiotensin 2 receptor antagonist or calcium antagonist or ACE inhibitor + calcium antagonist or angiotensin 2 receptor antagonist + calcium antagonist.

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Features of antihypertensive therapy in patients with diabetes

Whenever possible, an intensive regimen of non-drug interventions should be used in patients with type 2 diabetes, with particular attention to weight loss and limiting salt intake. Target blood pressure level is 130/80 mm Hg. Antihypertensive therapy is prescribed already with stage 1 hypertension. Diuretics and beta blockers should not be used at the first stage of treatment, because they aggravate insulin resistance and cause the need to increase the dose or number of glucose-lowering drugs.

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First-line drugs, in cases where monotherapy is sufficient, are ACE inhibitors or angiotensin 2 receptor blockers; they should also be a mandatory component of combination therapy (imidazole receptor antagonists, low-dose thiazide diuretics, beta-blockers (nebivolol) can be added to them or carvedilol), Ca channel blockers). Treatment decisions should consider the need for interventions that address all risk factors, including statins.

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Features of antihypertensive therapy in patients with impaired renal function

Renal dysfunction is always accompanied by a high risk of developing cardiovascular complications. To prevent the progression of renal dysfunction it is necessary: ​​it is necessary to achieve a target blood pressure level of less than 130/80 mm Hg. To achieve target blood pressure, a combination of several drugs (including loop diuretics) is often required. To reduce the severity of proteinuria, it is necessary to use angiotensin 2 receptor blockers, ACE inhibitors, or a combination thereof. In addition to antihypertensive therapy, such patients are shown statins and antiplatelet drugs, because they have a very high risk of developing cardiovascular complications.

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Features of antihypertensive therapy in patients with cerebrovascular pathology

Target blood pressure level is less than 140/90 mmHg. In such patients, all groups of antihypertensive drugs can be used. The most effective is the prescription of ACE inhibitors or angiotensin 2 receptor blockers in combination with diuretics.

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Features of antihypertensive therapy in patients with ischemic heart disease, CHF, atrial fibrillation

In post-MI patients, early administration of beta-blockers, ACE inhibitors, or angiotensin 2 receptor blockers reduces the risk of recurrent MI and death. When a history of hypertension in patients with CHF is indicated in antihypertensive therapy, it is advisable to include thiazide and loop diuretics, beta blockers, ACE inhibitors, angiotensin 2 receptor blockers, aldosterone receptor blockers. The use of Ca channel blockers should be avoided.

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In patients with atrial fibrillation, strict monitoring of antihypertensive therapy is necessary when treated with anticoagulants. The use of angiotensin 2 receptor blockers is considered preferable in patients with paroxysmal atrial fibrillation. With a permanent form of atrial fibrillation, beta-blockers and non-dihydropyridine calcium channel blockers (verapamil, diltiazem), which reduce the frequency of the ventricular rhythm, retain their importance.

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Indications for hospitalization

Indications for planned hospitalization: - The need for special, often invasive, research methods to clarify the diagnosis or form of hypertension; Difficulties in selecting drug therapy in patients with frequent GCs; Refractory hypertension. Indications for emergency hospitalization: HA that cannot be controlled at the prehospital stage; GC with severe manifestations of hypertensive encephalopathy; Complications of hypertension that require intensive care and constant medical supervision: cerebral stroke, subarachnoid hemorrhage, acute visual impairment, pulmonary edema, etc.

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Hypertensive crisis

a sudden increase in systolic and/or diastolic blood pressure to individually high values, accompanied by the appearance or intensification of disorders of the cerebral, coronary and renal circulation, as well as severe dysfunction of the autonomic nervous system.

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Predisposing factors for the development of GC

Neuropsychic stressful situations Intense physical activity Prolonged hard work without rest, associated with great responsibility, taking large amounts of water and salty food the day before Marked changes in meteorological conditions Impact of “acoustic” and “light” stress, leading to overstrain of the auditory and visual analyzers Alcohol abuse Consumption large amounts of coffee Heavy smoking Sudden withdrawal of beta-blockers Sudden cessation of treatment with clonidine Excessive mental stress accompanied by lack of sleep Treatment with corticosteroids, NSAIDs, tricyclic antidepressants, sympathomimetic amines

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Diagnostic criteria for GC

Relatively sudden onset Individually high blood pressure, with diastolic blood pressure usually exceeding 120-130 mm Hg. Presence of signs of dysfunction of the central nervous system, encephalopathy with general cerebral and focal symptoms and corresponding complaints of the patient Neurovegetative disorders Cardiac dysfunction of varying severity with subjective and objective manifestations Pronounced ophthalmological manifestations (subjective signs and changes in the fundus) New or worsened renal dysfunction

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Classification of Civil Codes

GCs are divided into 2 large groups: complicated (life-threatening) and uncomplicated (non-life-threatening). Complicated crises are characterized by a significant increase in blood pressure, severe, rapidly progressive damage to target organs, posing a threat to the life and health of the patient. Complicated hypertensive crises include the following clinical situations:

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Rapidly progressive or malignant hypertension with papilledema Cerebrovascular diseases: acute hypertensive encephalopathy ischemic stroke with severe hypertension hemorrhagic stroke subarachnoid hemorrhage Heart disease: acute dissection of an aortic aneurysm acute left ventricular failure acute myocardial infarction or the threat of its development unstable stenosis cardia condition after coronary artery bypass surgery Kidney diseases: acute glomerulonephritis renal crisis in systemic connective tissue diseases severe hypertension after kidney transplantation

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Excess of circulating catecholamines pheochromocytoma crisis interaction of food or drugs with MAO inhibitors use of sympathomimetic amines “rebound” hypertension after sudden cessation of treatment with antihypertensive drugs Eclampsia Surgical diseases: severe hypertension in patients requiring immediate surgery postoperative hypertension postoperative bleeding in the area of ​​vascular ligation severe , extensive burns to the body, severe nosebleeds, head injuries

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Uncomplicated GCs

are not accompanied by acute target organ damage and do not require immediate initiation of intensive antihypertensive therapy, because Blood pressure is reduced slowly over the course of a day.

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When medicinal treatment of GC is necessary to solve the following problems

1. Relief of increased blood pressure: determine the degree of urgency of starting treatment, select a drug and route of administration, establish the required rate of blood pressure reduction, determine the level of permissible blood pressure reduction. 2. Ensuring adequate monitoring of the patient’s condition during the period of lowering blood pressure: timely diagnosis of the occurrence of complications or excessive lowering of blood pressure is necessary. 3. Consolidation of the achieved effect: prescribe the same drug with which blood pressure was reduced, if impossible, other antihypertensive drugs, taking into account the mechanism and duration of action of the selected drugs. 4. Treatment of complications and concomitant diseases.

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Algorithm for choosing therapy for GC

Uncomplicated GC Treatment of uncomplicated GC can be carried out on an outpatient basis. In uncomplicated HA, the rate of blood pressure reduction should not exceed 25% in the first 2 hours, followed by reaching the target level within 24-48 hours. Drugs with a rapid onset of action and a short half-life should be used.

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Choice of drugs for uncomplicated GC

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Complicated HA is accompanied by life-threatening conditions and requires lowering blood pressure, starting from the first minutes, with the help of parenterally administered drugs. Patients are treated in the emergency cardiology department or the intensive care unit of the cardiology or therapeutic department. Blood pressure should be reduced gradually to avoid deterioration of blood supply to the brain, heart and kidneys, usually by no more than 25% in the first 1-2 hours.

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Hypertension is high and constant blood pressure: 140/90 and above.

The ideal level is when the top blood pressure number stays below 120 (systolic pressure). The bottom number should be below 80 (diastolic).

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Hypertension is the most common disease of the 21st century (WHO). Approximately 600 million people worldwide suffer from high blood pressure.

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Stages of hypertension

Stage 1 (mild) is characterized by relatively small increases in blood pressure in the range of 160-179(180) mm Hg. Art. systolic, 95-104 (105) mm Hg. Art.-diastolic. The blood pressure level is unstable, while the patient rests it gradually normalizes, but the disease is already fixed, the increase in blood pressure inevitably returns. Some patients do not experience any health problems. Others are worried about headaches, noise in the head, sleep disturbances, and decreased mental performance. Occasionally, non-systemic dizziness and nosebleeds occur. Usually there are no signs of left ventricular hypertrophy, the ECG deviates little from the norm, sometimes it reflects a state of hypersympathicotonia.

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Stage 2 (middle) differs from the previous one by a higher and stable level of blood pressure, which at rest is in the range of 180-200 mm Hg. Art. systolic and 105-114 mm Hg. Art. diastolic. Patients often complain of headaches, dizziness, and pain in the heart. Signs of target organ damage are detected: left ventricular hypertrophy, ECG signs of subendocardial ischemia. On the part of the central nervous system, various manifestations of vascular insufficiency are observed, and cerebral strokes are possible. In the fundus, in addition to narrowing of the arterioles, compression of the veins is observed. Renal blood flow and glomerular filtration rate are reduced, although urine tests are not abnormal.

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Stage 3 (severe) is characterized by a more frequent occurrence of vascular accidents, which depends on a significant and stable increase in blood pressure and the progression of atherosclerosis of larger vessels. Blood pressure reaches 200-230 mm Hg. Art. systolic, 115-129 mm Hg. Art. diastolic. There is no spontaneous normalization of blood pressure. The clinical picture is determined by damage to the heart (angina pectoris, myocardial infarction, circulatory failure, arrhythmias), brain (ischemic and hemorrhagic infarctions, encephalopathy), fundus, kidneys (decreased renal blood flow and glomerular filtration). Some patients with stage III hypertension, despite a significant and sustained increase in blood pressure, do not experience severe vascular complications for many years.

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Cause of hypertension

Statistics: 90% of hypertension diseases are caused by lifestyle and bad habits. Conclusion: we become hypertensive in most cases by our own choice.

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Lifestyle factors are the cause of hypertension

Excess body weight Every kilogram of fat requires 15 km of additional tiny blood vessels. Therefore, more pressure is required to push blood through them. Statistics: people with a body weight 20% higher than normal are 5 times more likely to suffer from hypertension than people with normal body weight. In 70% of men and 61% of women with hypertension, the cause of the disease was obesity.

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Excessive salt intake, excess dietary sodium It has been established that high blood pressure is rare in those regions of the globe where the salt content in food is very low. In many countries, salt consumption is constantly increasing. As a result, hypertension, as an epidemic, affects half of the adult population. Excess salt in the body often leads to spasm of the arteries, fluid retention in the tissues and, as a result, to the development of arterial hypertension. It is estimated that every kilogram of excess weight means an increase in blood pressure by 2 mm. rt. Art.

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Smoking Components of tobacco smoke enter the bloodstream and cause vasospasm. Substances contained in tobacco contribute to mechanical damage to the walls of the arteries, which predisposes to the formation of atherosclerotic plaques in this area. Smoking one cigarette increases blood pressure. The elevated blood pressure persists for at least 30 minutes.

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Alcohol The result of scientific research: moderate alcohol consumption (no more than 5 times a year) leads to hypertension in 15% of cases. Daily consumption of strong alcoholic drinks increases blood pressure by 5-6 mm. rt. Art. per year.

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Coffee, tea The result of scientific research: one cup of coffee or tea can increase blood pressure by 5-6 divisions.

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Inactivity The result of scientific research: a person who does not exercise will sooner or later suffer from high blood pressure.

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Stress and mental stress The stress hormone adrenaline causes the heart to beat faster, pumping a larger volume of blood per unit of time, as a result of which the pressure increases. If stress continues for a long time, then the constant load wears out the blood vessels and the increase in blood pressure becomes chronic.

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Atherosclerosis Excess cholesterol leads to loss of elasticity in the arteries, and atherosclerotic plaques narrow the lumen of blood vessels, which makes it difficult for the heart to function. All this leads to increased blood pressure. However, hypertension, in turn, spurs the development of atherosclerosis, so these diseases are risk factors for each other.

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Heredity Heredity plays an important role in the development of hypertension, mainly in young people, and less so in older people. It has been established that hypertension in families where immediate relatives suffer from high blood pressure develops several times more often than in members of other families. Children of parents with hypertension are 3.5 times more likely to suffer from it compared to other children. It is not hypertension itself that can be inherited genetically, but only a predisposition to it; this is due to the characteristics of the metabolism of certain substances (in particular, fats and carbohydrates), as well as neuropsychic reactions. However, the implementation of genetic predisposition is largely determined by external influences: living conditions, nutrition, unfavorable factors.

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Prevention of the development of hypertension Prevention of arterial hypertension is divided into primary and secondary. Primary prevention is needed for healthy people - those whose blood pressure does not yet exceed normal levels. The following set of health measures will help not only keep your blood pressure normal for many years, but also get rid of excess weight and significantly improve your overall well-being.

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Physical exercises Any physical exercises in people with mild and moderate arterial hypertension help improve physical performance. Exercises aimed at training endurance (general developmental exercises, breathing exercises, exercise equipment, swimming, brisk walking, running) lead to a noticeable antihypertensive effect. However, during intense physical activity, systolic pressure increases sharply, so it is best to exercise a little (30 minutes) each day, gradually increasing the intensity from light to moderate.

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Limiting animal fats Gradually replace butter, cheeses, sausages, sour cream, lard and fried cutlets with additional vegetables and fruits, vegetable oil and lean fish from your diet. Prefer low-fat dairy products. This way you can control cholesterol levels in the blood (prevention of atherosclerosis), normalize weight and at the same time enrich your diet with potassium, which is very useful for hypertension.

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Low-salt diet The amount of table salt should be limited to 5 grams (1 teaspoon) per day. It should be noted that many products (cheeses, smoked and pickled products, sausages, canned food, mayonnaise, chips) themselves contain a lot of salt. So, remove the salt shaker from the table and never add salt to ready-made dishes. Replace salt with herbs and garlic. If it is difficult to do without salt, you can purchase salt with a reduced sodium content, the taste of which is almost no different from regular salt.

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Psychological relief Stress is one of the main causes of increased blood pressure. That’s why it’s so important to master methods of psychological relief - auto-training, self-hypnosis, meditation. It is important to strive to see the positive sides in everything, to find joy in life, to work on your character, changing it towards greater tolerance for other people’s shortcomings, optimism, and balance. Hiking, sports, hobbies and spending time with pets also help maintain mental balance.

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Non-drug therapy In addition to the hypertensive diet, therapy may include breathing exercises, light massage, acupuncture, acupuncture, reflexology, sleep normalization, daily routine, taking natural and synthetic vitamins, antioxidants, nutritional supplements and restorative herbs. In short, it’s worthwhile to “improve” your lifestyle as much as possible. Measuring blood pressure Do this daily, and write down the resulting numbers in a special notebook. If your blood pressure approaches 140/90, or is higher than this figure, it means it is elevated and you should consult a doctor.

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Symptomatology of arterial hypertension syndromes, coronary insufficiency. Diagnostic signs of hypertension, symptomatic arterial hypertension, coronary heart disease.

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Arterial hypertension syndrome (AH) is a symptom complex, the main manifestation of which is an increase in blood pressure - systolic (SBP) and/or diastolic (DBP). According to WHO recommendations, SBP is considered elevated if it is equal to or higher than 140 mm Hg, DBP is 90 mm Hg. According to etiology, hypertension is divided into primary (hypertensive disease) and secondary (symptomatic) arterial hypertension.

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Hypertension (essential) is a disease in which an increase in blood pressure occurs in the absence of an obvious cause. Symptomatic hypertension is a condition in which the cause of increased blood pressure can be established.

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Rules for measuring blood pressure
blood pressure measurements must be carried out at rest, at least 2 times with an interval of 2-3 minutes, pressure is measured on both arms in both horizontal and vertical (sitting) positions. The highest blood pressure values ​​​​are taken into account, which more accurately correspond to intra-arterial blood pressure

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The most informative method for studying blood pressure is 24-hour blood pressure monitoring, which can help exclude “white coat” hypertension and make a differential diagnosis between symptomatic arterial hypertension

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The level of blood pressure is determined by the relationship between the cardiac minute vibration of the blood and peripheral vascular resistance. Cardiac blood output depends on the contractility of the left ventricle, and peripheral resistance depends on the tone of small vessels.

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Classification of hypertension according to blood pressure level
categories SBP, mm Hg. Art. DBP, mm Hg.
normotension normotension normotension
optimal normal high normal 130-139 85-89
hypertension hypertension hypertension
I Art. (soft AG) 140-159 90-99
II Art. (moderate) 160-179 100-109
III Art. (severe) ≥180 ≥110
Isolated SAG ≥140 ≤90

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Complaints of patients with arterial hypertension syndrome
Cerebral: headache (mainly in the occipital region), dizziness, tinnitus, noise in the head, flashing “spots” before the eyes, irritability (arise due to disturbances in vascular tone - either by dilation or by their spasm, as a result of which cerebral circulation is disrupted. A also due to irritation of cerebral vascular receptors by increased blood pressure). Cardiac: pain or discomfort in the heart area, palpitations, sometimes interruptions in the work of the heart (associated with a discrepancy between coronary blood flow and myocardial oxygen demand, since the heart works at an increased rate) General: weakness, decreased ability to work, sleep disturbance

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To establish the stage of arterial hypertension (both essential hypertension and symptomatic hypertension), a classification based on target organ damage is used. There are 3 stages of arterial hypertension

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Classification of hypertension according to target organ damage
Stage I: There are no objective signs of damage to target organs Stage II: There are objective signs of damage to target organs without clinical signs of dysfunction Heart - left ventricular hypertrophy (according to ECG, echocardiography, radiography), Fundus - generalized narrowing of the retinal arteries, Kidneys - microalbuminuria or proteinuria and/or a slight increase in plasma creatinine (in men 115-133 µmol/l or 1.3-1.5 mg/dl, in women 107-124 µmol/l or 1.2-1.4 mg /dl).

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Left ventricular hypertrophy

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Stage III - the presence of objective signs of damage to target organs with clinical manifestations of impairment of their function (stage of complications)
Heart – myocardial infarction, heart failure stage II-III. Brain - stroke, transient ischemic attack, acute hypertensive encephalopathy, chronic hypertensive encephalopathy stage III, vascular dementia Fundus - retinal hemorrhages and exudates with or without papilledema Kidneys - plasma creatinine concentration in men >133 µmol/l or >1.5 mg/dL, in women >124 µmol/L or 1.4 mg/dL Vessels – aortic dissection

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Hypertension Clinic
Stage I – characterized by an unstable increase in blood pressure, which is accompanied by cerebral, cardiac and general complaints. There are no objective signs other than increased blood pressure. Stage II – characterized by persistently elevated blood pressure and prolonged complaints, which tend to recur and progress. There are objective signs of target organ damage (cardiac impulse - strong, resistant, high; the left border of the heart is displaced outward due to left ventricular hypertrophy, weakening of the 1st tone and emphasis of the 2nd tone on the aorta; ECG and ultrasound signs of left ventricular hypertrophy), the appearance of hypertensive crises . It is enough to identify signs of damage to at least one target organ, regardless of the value of blood pressure. Stage III – characterized by a high and persistent increase in blood pressure and objective signs of complications from target organs, frequent hypertensive crises

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Hypertensive crisis (HC) is a sudden increase in SBP and DBP above individually normal values ​​in patients with hypertension or symptomatic hypertension, which is accompanied by pronounced objective changes in target organs.
There are 2 types of hypertensive crises according to the clinical development: adrenal crisis (type I) and noradrenal crisis (type II)

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Type I (adrenal) GK
Occurs more often in stages 1-2 of hypertension Characterized by a rapid onset (several hours) Predominant increase in systolic blood pressure Severe vegetative disorders (headache, body tremors, palpitations, sensation of flushing, heat, increased frequency of urination) On examination, facial hyperemia is determined Lasts several minutes or hours , does not always end in severe complications from target organs

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Type II (noradrenal) CG
Occurs in the late stages of hypertension Characterized by gradual development (tens of hours, days) Predominant increase in diastolic blood pressure Continues up to a day Often accompanied by complications from target organs - blurred vision, numbness of the extremities, nausea, vomiting (symptoms of cerebral edema), impaired coordination of movements, progression of heart failure, pulmonary edema, myocardial infarction, cardiac arrhythmia

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Secondary (symptomatic) arterial hypertension
Nephrogenic - renovascular (renal artery stenosis) - parenchymal kidney damage (pyelonephritis, glomerulonephritis, nephrosclerosis) - kidney damage with tuberculosis, tumors, sepsis, diffuse connective tissue diseases - with congenital kidney anomalies - with diabetic nephropathies, amyloidosis, glomerulosclerosis

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Endocrine hypertension
diffuse toxic goiter (Graves disease) pheochromocytoma primary aldosteronism Itsenko-Cushing syndrome acromegaly

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Hemodynamic (cardiovascular) hypertension
Coarctation of the aorta Atherosclerosis of the aorta and large vessels Complete atrioventricular block Aortic valve insufficiency Mitral insufficiency and others

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Neurogenic hypertension
Skull injuries Inflammatory diseases of the central nervous system Brain tumors

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Exogenous hypertension
Medicinal (use of corticosteroids, contraceptives) Nutritional (tyramine)

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Diagnosis verification
To establish a diagnosis of hypertension, it is necessary to exclude symptomatic arterial hypertension. A sudden, persistent and often refractory to antihypertensive therapy increase in blood pressure indicates the presence of secondary hypertension. The first detected increase in blood pressure in young (under 30) and over 60 years of age is more typical for symptomatic hypertension

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Coronary heart disease (CHD) is a group of diseases (angina pectoris, myocardial infarction, cardiosclerosis), which are based on a discrepancy between coronary blood flow and myocardial oxygen demand caused by atherosclerosis of the coronary arteries. The clinical classification distinguishes 5 classes of IHD. We will look at 3 types - stable angina (refers to chronic ischemic heart disease), unstable angina and myocardial infarction (acute ischemic heart disease).

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Risk factors for ischemic heart disease:
Hypercholesterolemia Arterial hypertension Physical inactivity Neuropsychic stress Diabetes mellitus Smoking Hereditary predisposition

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Angina pectoris (angina pectoris) is a common disease, the main clinical symptom of which is attacks of chest pain. In addition to atherosclerosis, the cause of angina pectoris can be coronary spasm (spasm of anatomically unchanged coronary arteries), caused by psycho-emotional or excessive physical stress.

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Pain details
Localization Irradiation Nature of pain Duration of pain What provokes pain How it is relieved What is accompanied Equivalent of pain
Behind the sternum, sometimes in the area of ​​the heart In the left half of the chest, arm, lower jaw, shoulder, shoulder blade, sometimes in the right arm Squeezing, pressing, baking from 3-5 to 20-30 minutes. Stress, physical activity, alcohol abuse, smoking, transition from a warm room to a cold one Nitroglycerin Weakness, sweating, fear of death (at the first attacks) Shortness of breath, weakness, compression of the entire chest

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Functional classes of stable angina
I FC – the occurrence of pain during increased physical activity (running, carrying significant weights) II FC – the occurrence of pain is provoked by walking on a flat road for more than 500 m, climbing more than 1 floor. Pain may occur in cold and windy weather. FC III – pain appears with slight exertion: walking on a flat road – 100-500 meters, climbing 1 floor. IV FC – minimal physical activity – walking up to 100 meters, attacks of pain at rest

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Signs of angina
Clinical signs of angina are not specific; Percussion and auscultation of the heart do not reveal any signs. Only recording an ECG during an attack of angina makes it possible to make the correct diagnosis. Signs of coronary blood flow disturbance are determined - ↓ST below the isoline, negative or smoothed T wave. After the end of the angina attack, the characteristic signs on the ECG disappear. Therefore, an appropriate diagnostic method is Holter ECG.

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Unstable angina - causes a transition from the chronic phase to the acute phase, as a result of activation of the atherosclerotic plaque, when the process of rapid thrombus formation begins. The criteria for the transition of stable angina to unstable are:
Increased frequency of angina pain attacks Prolongation of their duration Increased consumption of nitroglycenin

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Basic methods of examining patients with signs of coronary artery disease
ECG VEM, treadmill test Holter monitoring Coronary angiography - determination of the stage of narrowing and occlusion of the coronary arteries

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The extreme manifestation of IHD is myocardial infarction. Myocardial infarction (MI) is a disease that is manifested by the formation of a necrotic area in the heart muscle due to disruption of coronary blood flow. The main cause of MI is atherosclerosis of the coronary arteries (95%). Or due to embolism of the coronary artery in patients with septic endocarditis or thrombophlebitis, due to inflammatory lesions of the coronary arteries - rheumatic coronaritis, periarteritis nodosa.

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Myocardial infarction

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The pathological process occurs in the endothelium or intima of the coronary arteries. The thrombus formation system is activated and the atherosclerotic plaque ruptures. The collagen fibers of the plaque come into contact with platelets, which leads to aggregation and thrombus formation.

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Myocardial infarction goes through several stages in its development: I. – the most acute stage (corresponds to the period of myocardial ischemia) – lasts from 30 minutes to 2 hours and its manifestation is intense pain syndrome – pain behind the sternum or in the area of ​​the heart of a squeezing, pressing or cutting nature, of significant intensity lasting more than 30 minutes with radiation to the left arm , back, jaw, or covering the entire surface of the chest, accompanied by fear of death, decreased blood pressure, cold sticky sweat; not relieved by nitroglycerin. This is a typical anginal form of MI. (it was first described by Obraztsov and Strazhesko in 1909).

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The most acute stage of myocardial infarction
Giant T waves appear on the ECG, which are high-amplitude and pointed. They are signs of subendocardial damage; these areas are most sensitive to ischemia

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Atypical forms of myocardial infarction
Abdominal (gastralgic) - characterized by localized pain in the abdomen, mainly in the epigastrium, there may be nausea, vomiting, constipation. It is observed with MI of the posterior wall of the left ventricle. Asthmatic - begins with an attack of cardiac asthma and pulmonary edema without pain. The main manifestation is severe shortness of breath or suffocation. Arrhythmic - characterized by the sudden onset of rhythm disturbances or heart block without pain. Cerebral – manifested by cerebral circulation disorders. Painless – when the patient has no clinical signs of the disease.