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Presentation on the topic: Arterial hypertension
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Arterial hypertension is a stable increase in blood pressure - systolic to a value of 140 mm Hg and above and / or diastolic to a level of 90 mm Hg. st and higher according to the data of at least two measurements according to the Korotkoff method at two or more consecutive visits of the patient with an interval of at least 1 week. Arterial hypertension is a stable increase in blood pressure - systolic to a value of 140 mm Hg and above and / or diastolic to a level of 90 mm Hg. st and higher according to the data of at least two measurements according to the Korotkoff method at two or more consecutive visits of the patient with an interval of at least 1 week.
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There are essential (primary) and secondary arterial hypertension. Essential arterial hypertension is 90-92%, secondary - about 8-10% of all cases of high blood pressure. There are essential (primary) and secondary arterial hypertension. Essential arterial hypertension is 90-92%, secondary - about 8-10% of all cases of high blood pressure.
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a chronic disease of unknown etiology with a hereditary predisposition that occurs as a result of the interaction of genetic factors and environmental factors, characterized by a stable increase in blood pressure in the absence of damage to its regulatory organs and systems. a chronic disease of unknown etiology with a hereditary predisposition that occurs as a result of the interaction of genetic factors and environmental factors, characterized by a stable increase in blood pressure in the absence of damage to its regulatory organs and systems.
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if systolic and diastolic blood pressure levels fall into different classification categories, the higher category should be selected. if systolic and diastolic blood pressure levels fall into different classification categories, the higher category should be selected. As a criterion for diagnosing hypertension, the levels of systolic and diastolic blood pressure should be equally used; to determine the degree of isolated systolic hypertension, the gradations given in the column "systolic blood pressure" are used.
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WHO and MOAG experts proposed risk stratification into four categories (low, medium, high and very high) or risk 1, 2, 3, 4. WHO and MOAG experts 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 vascular diseases as well as myocardial infarction and stroke. To determine the degree of risk of developing cardiovascular complications, individual for a given patient, it is necessary to assess not only the degree of hypertension, but also the number of risk factors, the degree of damage to target organs and the presence of concomitant cardiovascular diseases.
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Cardiovascular disease risk factors Cardiovascular disease risk factors 1. Used for risk stratification Systolic and diastolic blood pressure values Age: men over 55 years women over 65 Smoking Total blood cholesterol level over 6.5 mmol/l Diabetes mellitus Familial cases early development SS diseases
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2. Other factors adversely affecting the prognosis 2. Other factors adversely affecting the prognosis Decreased HDL cholesterol Elevated LDL cholesterol Microalbuminuria (30-300 mg/day) in diabetes Impaired glucose tolerance Obesity Sedentary lifestyle Elevated blood fibrinogen levels Social- high-risk economic groups
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Target organ damage Target organ damage Left ventricular hypertrophy (ECG, echocardiography, Rtg) Proteinuria and/or slight increase in plasma creatinine Ultrasound or radiological signs of atherosclerotic lesions of the carotid, iliac, femoral arteries, aorta Generalized or focal narrowing of the retinal arteries
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Associated clinical conditions Associated clinical conditions Cerebrovascular disease: Ischemic stroke Hemorrhagic stroke Transient ischemic attacks Heart disease: MI Angina pectoris Coronary revascularization Congestive HF Renal disease: Diabetic nephropathy Renal failure Vascular disease: Dissecting aneurysm Symptomatic peripheral arterial disease Severe hypertensive retinopathy: Hemorrhage exudates Edema of the optic nipple
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Low risk group (risk 1). This group includes men and women younger than 55 years of age with hypertension in the absence of other risk factors, target organ damage and associated cardiovascular diseases. Low risk group (risk 1). This group includes men and women younger than 55 years of age with hypertension in the absence of other risk factors, target organ damage and associated cardiovascular diseases. Medium risk group (risk 2). This group includes patients with hypertension of 1 or 2 degrees. 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 CVS 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. This group also includes patients with grade 3 hypertension without other risk factors, without target organ damage, without concomitant diseases of CVS and DM. 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. This group also includes patients with grade 3 hypertension without other risk factors, without target organ damage, without concomitant diseases of CVS and DM. Very high risk group (risk 4). This group includes patients with any degree of hypertension, with concomitant diseases of the cardiovascular system, as well as with grade 3 hypertension with other risk factors and/or damage to target organs and/or diabetes, even in the absence of concomitant diseases.
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this is an increase in blood pressure, etiologically associated with certain, as a rule, clinically well-defined diseases of the organs and systems involved in the regulation of blood pressure. this is an increase in blood pressure, etiologically associated with certain, as a rule, clinically well-defined diseases of the organs and systems involved in the regulation of blood pressure.
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Secondary systolic-diastolic 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 kidney disease Kidney disease in systemic connective tissue diseases and systemic vasculitis Diabetic nephropathy Hydronephrosis Kidney tuberculosis Congenital hypoplephrosis of the kidneys Myeloma nephropathy Goodpasture
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1.2 Renovascular hypertension 1.2 Renovascular hypertension Atherosclerosis of the renal arteries Fibromuscular hyperplasia of the renal arteries Thrombosis of the renal arteries and veins Renal artery aneurysms Nonspecific aortoarteritis 1.3 Tumors of the kidneys producing renin 1.4 Primary renal retention of sodium (Liddle's syndrome) 1.5 Nephroptosis
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2. Endocrine 2. Endocrine Adrenal (s-m Itsenko-Cushing, congenital virilizing hyperplasia of the adrenal cortex, primary hyperaldosteronism, pheochromocytoma) Hypothyroidism Acromegaly Hyperparathyroidism Carcinoid 3. Coarctation of the aorta 4. AH during pregnancy
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5. Neurological disorders 5. Neurological disorders Increased intracranial pressure (brain tumor, encephalitis, respiratory acidosis) Quadriplegia Lead intoxication Acute porphyria Hypothalmic (diencephalic) s-m Familial dysautonomia Guillain-Barré s-m Sleep apnea of central origin
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6. Acute stress, including postoperative 6. Acute stress, including postoperative Psychogenic hyperventilation Hypoglycemia Burn disease Pancreatitis Withdrawal symptoms in alcoholism Crisis in sickle cell anemia Condition after resuscitation
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7. Hypertension induced by drugs, as well as exogenous intoxication Taking oral contraceptives 7. Hypertension induced by drugs, as well as exogenous intoxications Taking oral contraceptives Treatment with corticosteroids, mineralocorticoids, sympathomimetics, estrogens Treatment with monoamine oxidase inhibitors simultaneously with taking foods rich in tyramine Lead intoxication , thallium, cadmium 8. Increased BCC Excessive intravenous infusions Polycythemia vera 9. Alcohol abuse (chr. alcoholism)
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1. Increased cardiac output 1. Increased cardiac output Aortic valve insufficiency Arteriovenous fistula, open aortic duct C-m thyrotoxicosis Paget's disease Hypovitaminosis B Hyperkinetic type of hemodynamics 2. Sclerosed rigid aorta
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Arterial hypertension 1 tbsp. Risk 2. Dyslipidemia. Arterial hypertension 1 tbsp. Risk 2. Dyslipidemia. AG 2 tbsp. Risk 3. Hypertensive heart H1. Ventricular extrasystole. AG 2 tbsp. Risk 4. DM, type 2, stage of clinical and metabolic subcompensation, middle stage. severity, diabetic microangiopathy of the vessels of the lower extremities. AG 3 tbsp. Risk 4. IHD: exertional angina FC 2. Atherosclerosis of the aorta, coronary arteries. N 1. Polycystic kidney disease. Chr. pyelonephritis, without exacerbation. Secondary nephrogenic hypertension.
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After establishing the diagnosis of hypertension and assessing the cardiovascular risk, an individual patient management strategy is developed. After establishing the diagnosis of hypertension and assessing the cardiovascular risk, an individual patient management strategy is developed. Important aspects of managing a patient with hypertension are: Patient motivation for treatment and adherence to 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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Collection of anamnesis Collection of anamnesis to determine the duration of the increase in blood pressure, its levels, the presence of hypertensive crises; factors provoking rises in blood pressure; to clarify the presence of signs that allow to suspect the secondary nature of hypertension: a family history of renal disease; a history of kidney disease, bladder, hematuria, abuse of analgesics; the use of various drugs 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, seizures (aldosteronism)
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identify factors that aggravate the course of hypertension; identify factors that aggravate the course of hypertension: the presence of dyslipidemia, diabetes, and other diseases of the heart and blood vessels; burdened history of hypertension, diabetes, other CVD 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 patient complaints indicating damage to target organs: carefully identify patient complaints indicating damage to target organs: brain, eyes - the presence and nature of headache, dizziness, sensory and motor disorders, visual impairment; heart - chest pains, their connection with rises in blood pressure, emotional and physical loads, palpitations, interruptions in the work of the heart, shortness of breath; kidneys - thirst, polyuria, hematuria, nocturia; peripheral arteries - cold extremities, intermittent claudication. assess the possible impact on AH factors environment, marital status, nature of work; to clarify the medical, social and labor anamnesis.
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On physical examination, the clinician should look for POM and signs of secondary hypertension. On physical examination, the clinician should look for POM and signs of secondary hypertension. Be sure to measure the height, weight, waist circumference of the patient, calculate the BMI. The following data revealed during the examination may indicate the secondary nature of hypertension: Symptoms of the disease or Itsenko-Cushing's syndrome; Skin neurofibromatosis (s-m pheochromocytoma); Kidney enlargement (polycystic, volumetric formations); Weakened or delayed pulse on the femoral artery and a reduced level of blood pressure on it (coarctation of the aorta, nonspecific aortoarteritis); Rough systolic murmur over the aorta, in the interscapular region (coarctation of the aorta, aortic disease); Auscultation of the abdomen - noise over the area of the abdominal aorta, renal arteries (renal artery stenosis - renovascular hypertension).
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POM should be suspected in: POM should be suspected in: brain - auscultation of noises over the carotid arteries, motor and sensory disorders; retina - changes in the vessels of the fundus; heart - increased apex beat, rhythm disturbances, the presence of symptoms of CHF (wheezing in the lungs, the presence of peripheral edema, an increase in the size of the liver); peripheral arteries - absence, weakening or asymmetry of the pulse, cold extremities, symptoms of skin ischemia; carotid arteries - systolic murmur over the area of the arteries.
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Fasting plasma glycemia Fasting plasma glycemia Glucose tolerance test Total CL LDL CL HDL CL TG Potassium Uric acid Creatinine Estimated creatinine clearance or glomerular filtration rate Hemoglobin and hematocrit Urinalysis (determining microalbuminuria); quantitative analysis proteinuria.
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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. 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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Antihypertensive therapy should be continuous; 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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The effectiveness of antihypertensive therapy is assessed by the level of blood pressure reduction. 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 II receptor blockers and beta-blockers. These classes of drugs can be used as monotherapy or as low-dose fixed combinations.
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Regardless of the choice of drugs, the use of monotherapy can achieve the desired level only in a limited number of patients. Most patients require more than one antihypertensive drug to achieve their BP target. Initial therapy can be carried out with the help of both monotherapy and the combined use of two drugs at low doses, followed by an increase in the dose or number of drugs if necessary. The use of monotherapy as an initial one 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 level of blood pressure corresponds to 2 or 3 degrees of hypertension or the overall risk of complications is high. Regardless of the choice of drugs, the use of monotherapy can achieve the desired level only in a limited number of patients. Most patients require more than one antihypertensive drug to achieve their BP target. Initial therapy can be carried out with the help of both monotherapy and the combined use of two drugs at low doses, followed by an increase in the dose or number of drugs if necessary. The use of monotherapy as an initial one 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 level of blood pressure corresponds to 2 or 3 degrees of hypertension or the overall risk of complications is high.
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A combination of drugs in a fixed dose is preferred, since the simplification of treatment has a greater chance of adherence to therapy. A combination of drugs in a fixed dose is preferred, since the simplification of treatment has a greater 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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Whenever possible, an intensive regimen of non-pharmacological interventions should be used in patients with type 2 diabetes, with particular attention to weight loss and restriction of intake. table salt. Whenever possible, an intensive regimen of non-pharmacological interventions should be used in patients with type 2 diabetes, with particular attention to weight loss and restriction of salt intake. The target level of blood pressure is 130/80 mm Hg. Antihypertensive therapy is prescribed already with arterial hypertension 1 tbsp. Diuretics and beta-blockers should not be used at the first stage of treatment, because. they exacerbate insulin resistance and necessitate an increase in the dose or number of hypoglycemic 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 or carvedilol), Ca-channel blockers). 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 or carvedilol), Ca-channel blockers). The choice of treatment tactics should take into account the need for interventions that affect all risk factors, including the use of statins.
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Impaired kidney function is always accompanied by a high risk of developing CVD. Impaired kidney function is always accompanied by a high risk of developing CVD. To prevent the progression of impaired renal function, it is necessary: it is necessary to achieve the target level of blood pressure less than 130/80 mm Hg. A combination of several drugs (including loop diuretics) is often required to achieve target blood pressure. To reduce the severity of proteinuria, the use of angiotensin 2 receptor blockers, ACE inhibitors, or a combination thereof is necessary. In addition to antihypertensive therapy, statins and antiplatelet agents are indicated for such patients, because. they have a very high risk of developing CVD.
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In post-MI patients, early administration of beta-blockers, ACE inhibitors, or angiotensin II receptor blockers reduces the risk of recurrent MI and death. In post-MI patients, early administration of beta-blockers, ACE inhibitors, or angiotensin II receptor blockers reduces the risk of recurrent MI and death. When indicated in the anamnesis in patients with CHF for hypertension, it is advisable to include thiazide and loop diuretics, beta-blockers, ACE inhibitors, angiotensin II receptor blockers, and aldosterone receptor blockers in antihypertensive therapy. The use of Ca-channel blockers should be avoided.
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In patients with atrial fibrillation, strict control of antihypertensive therapy is necessary when treated with anticoagulants. In patients with atrial fibrillation, strict control of antihypertensive therapy is necessary when treated with anticoagulants. The appointment of angiotensin II receptor blockers is considered preferable in patients with paroxysms of 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 value.
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Indications for planned hospitalization: Indications for planned hospitalization: - The need for special, often invasive, research methods to clarify the diagnosis or form of hypertension; Difficulties in the selection of drug therapy in patients with frequent GC; Refractory AH. Indications for emergency hospitalization: GC, not stopped at the prehospital stage; GC with severe manifestations of hypertensive encephalopathy; Complications of hypertension requiring intensive care and constant medical supervision: cerebral stroke, subarachnoid hemorrhage, acute visual impairment, pulmonary edema, etc.
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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. 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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Neuropsychic stressful situations Neuropsychic stressful situations Intense physical activity Long-term hard work without rest, associated with great responsibility, taking large amounts of water and salty food the day before Pronounced changes in meteorological conditions Impact of "acoustic" and "light" stresses, leading to an overstrain of auditory and of visual analyzers Alcohol abuse Drinking large amounts of coffee Intensive smoking Sudden withdrawal of beta-blockers Sudden cessation of clonidine treatment Excessive mental stress, accompanied by lack of sleep Treatment of corticosteroids, NSAIDs, tricyclic antidepressants, sympathomimetic amines
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Relatively sudden onset Relatively sudden onset Individually high BP, with diastolic BP typically above 120-130 mmHg. Presence of signs of CNS dysfunction, encephalopathy with cerebral and focal symptoms and corresponding complaints of the patient
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GCs are divided into 2 large groups: complicated (life-threatening) and uncomplicated (non-life-threatening). 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 that pose 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 Rapidly progressive or malignant hypertension with papilledema Cerebrovascular disease: 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 impending myocardial infarction unstable angina condition after coronary bypass surgery Kidney disease: acute glomerulonephritis renal crisis in systemic connective tissue diseases severe hypertension after kidney transplantation
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Excess circulating catecholamines Excess circulating catecholamines crisis pheochromocytoma interaction of food or drugs with MAO inhibitors use of sympathomimetic amines "rebound" hypertension after abrupt discontinuation of antihypertensive drugs Eclampsia Surgical diseases: severe hypertension in patients requiring immediate surgery postoperative hypertension postoperative bleeding in the area ligation of vessels severe, extensive body burns severe nosebleeds head injuries
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1. Stopping the increase in blood pressure: determine the degree of urgency to start treatment, choose the drug and the route of its administration, set the required rate of blood pressure reduction, determine the level of acceptable blood pressure reduction. 1. Stopping the increase in blood pressure: determine the degree of urgency to start treatment, choose the drug and the route of its administration, set the required rate of blood pressure reduction, determine the level of acceptable blood pressure reduction. 2. Ensuring adequate control over the patient's condition during the period of lowering blood pressure: timely diagnosis of the occurrence of complications or excessive reduction in blood pressure is necessary. 3. Consolidation of the achieved effect: prescribe the same drug that lowered blood pressure, if not possible - other antihypertensive drugs, taking into account the mechanism and duration of the selected drugs. 4. Treatment of complications and concomitant diseases.
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Complicated GC Complicated GC 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 a cardiology emergency department or an intensive care unit in a cardiology or internal medicine department. Blood pressure should be reduced gradually, in order to avoid deterioration in the blood supply to the brain, heart and kidneys, as a rule, by no more than 25% in the first 1-2 hours.
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The most rapid decrease in blood pressure is necessary for dissecting aortic aneurysm (by 25% of the initial one in 10-15 minutes, the optimal time to reach the target SBP of 100-110 mm Hg is 20 minutes), as well as for acute left ventricular failure. The most rapid decrease in blood pressure is necessary for dissecting aortic aneurysm (by 25% of the initial one in 10-15 minutes, the optimal time to reach the target SBP of 100-110 mm Hg is 20 minutes), as well as for acute left ventricular failure. Patients with cerebrovascular complications require a special approach because excessive and / or rapid decrease in blood pressure contributes to an increase in cerebral ischemia. In the acute period of a stroke, the question of the need to reduce blood pressure and its optimal value is decided jointly with a neurologist individually for each patient.
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Symptomatology of syndromes of arterial hypertension, coronary insufficiency. Diagnostic signs of hypertension, symptomatic arterial hypertension, coronary heart disease.
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The syndrome of arterial hypertension (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 to be elevated equal to or above 140 mm Hg, DBP - 90 mm Hg. According to the etiology, hypertension is divided into primary (hypertension) 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 an increase in blood pressure can be identified.
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Rules for measuring blood pressure
measurement of blood pressure should be carried out at rest, at least 2 times with an interval of 2-3 minutes, pressure is measured on both hands both in a horizontal and vertical (sitting) position The highest blood pressure values are taken into account, which more closely correspond to intra-arterial blood pressure
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The most informative method for studying blood pressure is daily monitoring of blood pressure, with the help of which it is possible to exclude white-coat hypertension, to conduct a differential diagnosis between symptomatic arterial hypertension.
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The level of arterial pressure is determined by the ratio between cardiac minute blood circulation and peripheral vascular resistance. Cardiac output of blood depends on the contractility of the left ventricle, and peripheral resistance - due to the tone of small vessels.
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Classification of hypertension according to the level of blood pressure
CAD category, mm Hg Art. DBP, mm Hg
normotension normotension normotension
optimal normal high normal 130-139 85-89
hypertension hypertension hypertension
I st. (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, flickering of “flies” before the eyes, irritability (they occur due to a violation of vascular tone - either by expansion or by their spasm, as a result of which cerebral circulation is disturbed. A also due to irritation of the receptors of cerebral vessels by elevated blood pressure). Cardiac: pain or discomfort in the region of the heart, palpitations, sometimes interruptions in the work of the heart (associated with a mismatch between coronary blood flow and myocardial oxygen demand, since the heart works in an increased mode) 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 is applied according to target organ damage. There are 3 stages of arterial hypertension.
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Classification of hypertension by 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 impaired function 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 impaired function (stage of complications)
Heart - myocardial infarction, heart failure ІІ-ІІІ st. Brain - stroke, transient ischemic attack, acute hypertensive encephalopathy, stage III chronic hypertensive encephalopathy, 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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Clinic of hypertension
Stage I - characterized by an intermittent increase in blood pressure, which is accompanied by cerebral, cardiac and general complaints. There are no objective signs other than an increase in blood pressure. Stage II - characterized by consistently elevated blood pressure and long-term complaints that tend to recur and progress. There are objective signs of damage to target organs (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 magnitude 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 developmental clinic: adrenal crisis (type I) and noradrenal crisis (type II)
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Type I (adrenal) HA
It occurs more often in stages I-II of hypertension It is characterized by a rapid onset (several hours) Predominant increase in systolic blood pressure Severe vegetative disorders (headache, body trembling, palpitations, sensation of hot water, fever, increased frequency of urination) On examination, face hyperemia is determined Lasts several minutes or hours , does not always end in gross complications from the target organs
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II type (noradrenal) CG
Occurs in the late stages of hypertension Characterized by gradual development (tens of hours, days) Predominant increase in diastolic blood pressure Lasts up to a day Often accompanied by complications from target organs - visual impairment, numbness of the extremities, nausea, vomiting (symptoms of cerebral edema), impaired coordination of movements, progression of heart failure, pulmonary edema, myocardial infarction, cardiac arrhythmias
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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 anomalies of the kidneys - with diabetic nephropathy, amyloidosis, glomerulosclerosis
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Endocrine hypertension
diffuse toxic goiter (Basedow's disease) pheochromocytoma primary aldosteronism Itsenko-Cushing's syndrome acromegaly
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Hemodynamic (cardiovascular) hypertension
Coarctation of the aorta Atherosclerosis of the aorta and large vessels Complete atrioventricular blockade Aortic valve insufficiency Mitral insufficiency and others
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Neurogenic hypertension
Injuries of the skull Inflammatory diseases of the central nervous system Brain tumors
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Exogenous hypertension
Medication (use of corticosteroids, contraceptives) Alimentary (tyramine)
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Verification of the diagnosis
To establish the diagnosis of hypertension, it is necessary to exclude symptomatic arterial hypertension. Sudden, persistent and often refractory to antihypertensive therapy, an 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 characteristic of symptomatic hypertension
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Coronary artery disease (CHD) is a group of diseases (angina pectoris, myocardial infarction, cardiosclerosis), which are based on a mismatch between coronary blood flow and myocardial oxygen demand, caused by atherosclerosis of the coronary arteries. Clinical classification distinguishes 5 classes of coronary artery disease. We will consider 3 varieties - stable angina (refers to chronic coronary heart disease), unstable angina and myocardial infarction (acute coronary artery disease).
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Risk factors for coronary artery disease:
Hypercholesterolemia Arterial hypertension Hypodynamia Neuropsychic overstrain Diabetes mellitus Smoking Hereditary predisposition
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Angina pectoris is a common disease, the main clinical symptom of which is attacks of retrosternal pain. In addition to atherosclerosis, the cause of angina pectoris can be coronary spasm (spasm of anatomically unchanged coronary arteries), due to psycho-emotional or excessive physical overstrain.
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Detailing the pain
Localization Irradiation Nature of pain Duration of pain What provokes the onset of pain What is removed What is accompanied by Pain equivalent
Behind the sternum, sometimes in the region of the heart In the left half of the chest, arm, lower jaw, shoulder, shoulder blade, sometimes in the right arm Constricting, pressing, baking from 3-5 to 20-30 minutes. Stress, physical activity, alcohol abuse, smoking, transition from warm to cold environment 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
І FC - the occurrence of pain during increased physical exertion (running, carrying significant weights) ІІ FC - the occurrence of pain is provoked by walking on a flat road more than 500 m, lifting above 1 floor. The pain may appear in cold and windy weather. ІІІ FC - pain appears with a slight load: walking on a flat road - 100-500 meters, climbing to the 1st floor. ІV FC - minimal physical activity - walking up to 100 meters, attacks of pain at rest
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Signs of angina pectoris
Clinical signs of angina pectoris are not specific; percussion, auscultation of the heart signs are not detected. Only an ECG recording during an angina attack makes it possible to make a correct diagnosis. Signs of impaired coronary blood flow are determined - ↓ST below the isoline, negative or smoothed T wave. After the completion of an angina attack characteristics disappear on the ECG. Therefore, an expedient diagnostic method is Holter-ECG.
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Unstable angina causes the transition from the chronic to the acute phase, as a result of the activation of an atherosclerotic plaque, when the process of rapid thrombus formation starts. The criteria for the transition of stable angina to unstable are:
Increased frequency of angina attacks Lengthened their duration Increased nitroglycenin intake
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The main methods of examination of patients with signs of coronary artery disease
ECG VEM, treadmill test Holter monitoring Coronary angiography - determination of the degree of narrowing and occlusion of the coronary arteries
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The ultimate 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 impaired 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, on the basis of 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. There is an activation of the thrombus formation system, a rupture of an atherosclerotic plaque. Plaque collagen fibers come into contact with platelets, which leads to aggregation and thrombus formation.
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Myocardial infarction in its development goes through several stages: I. - the most acute stage (corresponding to the period of myocardial ischemia) - lasts from 30 minutes to 2 hours and its manifestation is an intense pain syndrome - pain behind the sternum or in the region of the heart of a compressive, pressing or cutting nature, of significant intensity lasting more than 30 minutes with irradiation to the left hand , back, jaw, or covering the entire surface of the chest, accompanied by a fear of death, a decrease in blood pressure, cold sticky sweat; not relieved by nitroglycerin. This is a typical - anginal form of MI. (was first described by Obraztsov and Strazhesko in 1909).
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The most acute stage of MI
Giant T waves appear on the ECG, which are high-amplitude, peaked. They are signs of a subendocardial lesion, it is these zones that are most sensitive to ischemia.
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Atypical forms of myocardial infarction
Abdominal (gastralgic) - characterized by localization of pain in the abdomen, mainly epigastric pain, there may be nausea, vomiting, constipation. 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 disorders of cerebral circulation. Painless - when the patient has no clinical signs of the disease.
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Arterial hypertension is an increase in systolic blood pressure up to 140 mm Hg. Art. and above and / or diastolic blood pressure up to 90 mm Hg. Art. and above, if such an increase is confirmed by repeated measurements of blood pressure. Essential or primary hypertension is a disease characterized by a persistent increase in blood pressure in the absence of an obvious reason for its increase (diagnosed in 90-95% of cases). Secondary hypertension (symptomatic arterial hypertension) is hypertension, the cause of which can be established (diagnosed in 5-10% of cases).
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Heredity. 60 genes involved in the development of hypertension have been identified, especially the polymorphism of the angiotensin-II-converting enzyme gene, angiotensinogen, renin, and glucocorticoid receptors. Overweight The relationship between hypertension, hyperinsulinemia and lipid metabolism disorders (decrease in high density lipoproteins, increase in low and very low density lipoproteins) and obesity - “metabolic syndrome” has been shown. Diabetes mellitus In diabetes mellitus (especially type II) AH occurs 2 times more often than in persons without it. Age Consumption of table salt more than 5 g/day Consumption of alcohol, coffee, smoking. Acute stressful situations, prolonged stress lead to an increase in blood pressure. A sedentary lifestyle increases the risk of hypertension by 20-50%. Environmental factors - noise, vibration, pollution, mild drinking water. RISK FACTORS OF AH
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Renin-angiotensin system of the myocardium and coronary vessels Tissue AII VESSELS MACROPHAGE FIBROBLAST MYOCYTE NERVE TERMINATION ACE Chymase Norepinephrine AI AII ACE AT1R AT2R AT1R AT2R AT1R MAST CELL Contractility Hypertrophy Chronotropism Apoptosis Fibrosis Am J Cardiol 2001; 88:1 L
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RAAS Kallikrein-kinin system Pressor system Regulation of blood circulation Sodium and water retention Hypertrophy, proliferation Fibrosis Activation of the coagulation system Stimulation of aldosterone secretion Stimulation of sympathetic activity Weakening of the baroreceptor mechanism Activation of the center of the vagus nerve Depressor system Regulation of microcirculation Natriuresis and diuresis Cytoprotection Slowdown of fibrosis Activation of the fibrinolytic system Stimulation of secretion in renin and prostaglandin systems Vascular permeability Circulatory bed Short-term effects Compensatory-adaptive reactions Tissue level Long-term effects Structural reorganization of target organs
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X-ray at GB determine the signs of left ventricular hypertrophy, its hypertrophy with dilatation, atherosclerotic lesions of the aorta, signs of venous congestion in the lungs (Fig. a, b, c).
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Pronounced hypertrophy of the left ventricle of the heart. An increase in the R wave in leads V5 - V6 and the S wave in leads V1, V2, while RV4< RV6, S в VI + R в V5 >35 mm, R in VI + S in V3 > 25 mm. Shift of the transition zone to the right to V3. Displacement of the electrical axis of the heart to the left, with RI > 12 mm. Skew-down bias segment S-T and T-wave inversion in I, aVL, V5, V6.
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Classification of arterial hypertension according to the level of arterial pressure (WHO, MOG, 1999) BP, mm Hg. Art. systolic diastolic Optimal pressure
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Stages of arterial hypertension depending on the damage to target organs (WHO, 1996) I st. There are no signs of target organ damage. II Art. One of the signs of target organ damage is present: left ventricular hypertrophy; generalized or focal vasoconstriction of the retina (hypertensive retinal angiopathy); microalbuminuria; atherosclerotic vascular changes (plaques) in the carotid arteries, aorta, iliac and femoral arteries; III Art. - In addition to the listed signs of target organ damage, there are also clinical manifestations: heart - angina pectoris, myocardial infarction, heart failure; brain - stroke, TNMK, hypertensive encephalopathy, vascular dementia; vessels - dissecting aortic aneurysm; manifestations of occlusive lesions of the peripheral arteries of the kidney - plasma creatinine concentration of more than 2 mg / 100 ml or 0.177 mmol / l, renal failure; retina - hypertensive retinopathy.
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Mechanisms of hypotensive action of β-blockers Level Nature of action of the CNS Block β-adrenergic receptors, increase the effect of NA on α-adrenergic receptors of the medulla oblongata with inhibition of the activity of the sympathetic nervous system. β-adrenergic receptors 1. High sensitivity to β-adrenergic receptors, competitive antagonism. 2. Membrane stabilizing activity. 3. Selectivity - a selective effect on the β1-receptors of the heart (cardioselectivity). Non-selective β-blockers act on β1-receptors of the heart and β2-receptors of blood vessels, kidneys, bronchi, and smooth muscles. Hemodynamics Negative chronotropic, inotropic effects, decrease in cardiac output, myocardial oxygen consumption, coronary blood flow. The initial increase in OPPS, with long-term therapy, vascular adaptation and normalization of peripheral resistance occur. Neuro-moral systems Reduce renin activity. Increase insulin release, decrease glucagon secretion.
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Classification and doses of β-blockers Drug Dose (mg/day) Frequency of administration per day Cardioselective without internal sympathomimetic activity Atenolol 25 - 100 1-2 Metoprolol 50 - 200 1 - 2 Nebivolol 2.5 - 5.0 1 with internal sympathomimetic activity Talinolol 150 - 600 3 Non-cardioselective without internal sympathomimetic activity Propranolol 20-160 2 - 3 with internal sympathomimetic activity Oxprenolol 20 - 480 2 - 3 with -adrenergic blocking properties Carvediol 25 - 100 1 Labetalol 200 - 1200 2
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Systemic effects of ACE inhibitors Effects Effects Cardioprotective effect regression of LVH and myocardiofibrosis; prevention of left ventricular dilatation; anti-ischemic effect; afterload reduction due to arterial vasodilation; reduced preload due to venous vasodilation; antiarrhythmic effect in myocardial ischemia. Vaso-protective effect suppression of proliferation of arterial smooth muscle cells; increased endothelium-dependent vasodilation; potentiation of the vasodilator effect of nitrates; improvement of regional hemodynamics. Reno-protective effect increased diuresis, natriuresis, potassium-sparing effect; increased blood flow in the medulla of the kidneys. Metabolic effects improved glucose metabolism by increasing the sensitivity of peripheral tissues to insulin; anti-atherogenic effect.
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Therapeutic doses of ACE inhibitors Name of the drug Therapeutic dose (mg / day) Frequency of administration Captopril 50-150 2 Enalapril (Renitec) 2.5-40 1-2 Lisinopril 5-40 1 Cilazapril 1.25-5 1-2 Ramipril 1.25 -20 1 Quinapril 5.0-8.0 1-2 Benazepril 2.5-5.0 1-2 Fosinapril 10-40 1-2 Spirapril 12.5-50 1-2 Perindopril (prestarium) 1.0-16 1-2
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Classification and doses of calcium antagonists Drugs Therapeutic dose (mg/24 h) Frequency of administration per day I Dihydropyridines 1 Nifedipine 30-120 3-4 2 Amlodipine 5-10 1 3 Lacidipine 2-8 1 II Benzodiazepines 1 Diltiazem (cardyl) 60-120 3 - 4 2 Long acting diltiazem 180-360 1
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The mechanism of action of AT1 receptor blockers is to eliminate the effects of angiotensin II mediated by AT1 receptors and enhance the effects of stimulation of AT2 receptors. DOSES OF AT1 RECEPTOR BLOCKERS Indications for administration are similar to those of ACE inhibitors. Side effects: headache, cough, development of mild hyperkalemia (losartan). Contraindications to the appointment of AT1 receptor blockers: pregnancy, hyperkalemia, bilateral renal artery stenosis. Drug name Daily dose (mg) Frequency of administration per day (24 hours) Irbesartan 300 1-2 Losartan 50-100 1-2 Telmisartan 80-160 1 Valsartan 80-160 1 Candesartan 8-16 1 Eprosartan 400-800 1-2
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Classification and doses of diuretics Name Daily dose, mg Thiazide diuretics Hydrochlorothiazide (dichlothiazide, hypothiazide) 12.5–50 Thiazide-like diuretics Clopamid 10–20 Indapamide (arifon) 1.5–2.5 Loop diuretics Furosemide 20–480 Ethacrynic acid (uregit) 25 - 100 Potassium-sparing diuretics Spironolactone (veroshpiron) 25 - 100 Amiloride 5 - 10
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Classification and doses of α-adrenergic blockers α1-Blocking action has dihydroergocristine, droperidol, carvedilol, labetalol. Name of the drug Release form, dose Daily dose (mg) Non-selective α-adrenergic blockers Pirroksan tab. 0.015 amp. 1.0 ml 1% solution 0.06-0.18 2-3 ml s.c., i.m.; Selective α1-blockers Prazosin tab. 0.0005 caps. 0.0001 0.0015 – 0.003 0.003 Doxazosin (carduran) tab. 2-4 mg 1-15 Terazosin (cornam) tab. 2-5 mg Bendazolol (gliofen) 1 tab. 20 mg
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DEATH QUARTET "OBESITY, HYPERTENSION, IMPAIRED GLUCOSE TOLERANCE, DYSLIPIDEMIA AND THEIR POSSIBLE RELATION TO INSULIN RESISTANCE" (C. Isles, 1997) obesity insulin resistance hypertension dyslipidemia glucose intolerance
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A hypertensive crisis is a sudden significant increase in blood pressure, accompanied by the appearance or intensification of disorders of the target organs and the autonomic nervous system. Criteria for a crisis: - sudden onset, - a significant increase in blood pressure, - the appearance or intensification of symptoms from the target organs. Classification of hypertensive crises recommended by the Ukrainian Society of Cardiology (2000). I. Complicated crises (with acute or progressive damage to target organs, pose a direct threat to the life of the patient, require immediate, within 1 hour, lowering blood pressure). II. Uncomplicated crises (without acute or progressive damage to target organs, pose a potential threat to the life of the patient, require a rapid, over several hours, decrease in blood pressure).
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ВИДЫ ОСЛОЖНЕННЫХ ГИПЕРТЕНЗИВНЫХ КРИЗОВ: Инфаркт миокарда Инсульт Острая расслаивающая аневризма аорты Острая недостаточность левого желудочка Нестабильная стенокардия Аритмии (пароксизмы тахикардии, мерцательной тахиаритмии, желудочковой экстрасистолии) Транзиторная ишемическая атака Эклампсия Острая гипертензивная энцефалопатия Кровотечение Острая почечная недостаточность ВИДЫ НЕОСЛОЖНЕННЫХ ГИПЕРТЕНЗИВНЫХ КРИЗОВ - Церебральный неосложненный криз - Гипоталамический paroxysm (diencephalic-vegetative crisis). - Cardiac uncomplicated crisis. - Increase in SBP up to 240 or DBP up to 140 mm Hg. - A significant increase in blood pressure in the early postoperative period.
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Treatment of complicated hypertensive crises Drug Method of administration Onset of action Duration of action Remarks Vasodilators lenno 1-3 min Suitable for immediate reduction of blood pressure when monitoring blood pressure. Nitroglycerin IV drip, 50-200 mcg/min After 2-5 minutes 5-10 minutes Particularly effective in acute heart failure Verapamil IV, 5-10 mg, continue IV drip 3-25 mg/h After 1-5 minutes 30-60 minutes Do not use in patients with heart failure and in those receiving β-blockers. Enalaprilat IV 1.25-5 mg After 15-30 minutes 6-12 hours Effective in acute left ventricular failure Nimodipine IV drip, 15 µg/kg in 1 hour, then 30 µg/kg in 1 hour After 10-20 min 2-4 hours For subarachnoid hemorrhages
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Treatment of complicated hypertensive crises Name of the drug Method of administration Onset of action Duration of action Remarks aortic aneurysm and coronary syndrome Esmolol IV drip 250-500 mcg/kg in 1 min for 1 min, then 50-100 mcg/kg in 4 min after 1-2 min 10-20 min Drug of choice for dissecting aortic aneurysm and postoperative hypertension Other drugs Furosemide IV bolus, 40-200 mg After 5-30 minutes 6-8 hours In hypertensive crises with acute heart or kidney failure Magnesium sulfate IV bolus, 5-20 ml 25% solution Through 30-40 min 3-4 h For convulsions, eclampsia of pregnancy
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Drugs for the treatment of uncomplicated hypertensive crises Drugs Doses and routes of administration Onset of action Side effects Clonidine 0.075-0.15 mg orally or 0.01% solution 0.5-2.0 IM or IV After 10-60 minutes Dry mouth, drowsiness, contraindicated in patients with A-B blockade, bradycardia Captopril 12.5-25 mg orally or sublingually After 30 minutes Hypotension in patients with renin-dependent hypertension IV After 10-20 minutes General weakness Nifedipine 5-10 mg orally or sublingually After 15-30 minutes Headache, tachycardia, redness, angina pectoris Diazepam 0.5% solution 1.0-2.0 IM Through 15-30 min Dizziness, drowsiness Prazosin 0.5-2 mg orally After 30-60 min Orthostatic hypotension, tachycardia Labetolol 200-400 mg orally After 30-60 min Orthostatic hypotension, bronchoconstriction Propranolol 20-80 mg orally After 30-60 min Tachycardia, bronchoconstriction Metoprolol 25-50 mg orally After 304-60 minutes Tachycardia, bronchoconstriction
Authors: Prof. Fazlyeva R. M. Assoc. Mukhetdinova G. A. Ufa,
Arterial hypertension (AH) is a condition in which systolic blood pressure is 140 mm Hg. Art. and above and / or diastolic blood pressure - 90 mm Hg. Art. and higher.
The prevalence of hypertension affects 20-30% of the adult population Among people over 65 years old - 50-65% The rule of half - half of the patients know about the presence of hypertension, half of those who know are treated, no more than half of those treated reach normal blood pressure levels.
Hypertension (essential or primary hypertension) is a chronic disease, the main manifestation of which is arterial hypertension syndrome in the absence of a primary cause for its increase. Frequency 90-95%.
HBetiology and pathogenesis Obesity Stress Genetic factors Excessive salt intake Membrane disorders Baro- and chemoreceptors. Endothelin RAAS Violation of sodium excretion. Increased SAS activity
Secondary hypertension (symptomatic) EG must be differentiated from secondary (symptomatic) hypertension, which is understood as such forms of increased blood pressure, which are caused by diseases of the organs and systems involved in the regulation of blood pressure.
The main groups of secondary hypertension: 1. Renal (nephrogenic) - 18% or 70-80% of symptomatic hypertension; 2. Endocrine; 3. Hemodynamic, caused by lesions of the heart, aorta, its large branches; 4. Centrogenic, caused by organic lesions of the central nervous system; 5. Exogenous, due to medication (GCS, hormonal contraceptives), alimentary (tyramine). A special form of hypertension is an increase in blood pressure due to an increase in blood viscosity, for example, with polycythemia.
Classification of symptomatic hypertension (according to Arabidze (1992) 1 Renal arterial hypertension 1) Congenital anomalies of the kidneys and blood vessels (hypoplasia, dystopia, hydronephrosis, polycystic, horseshoe kidney, pathological mobility, atresia and hypoplasia of the renal artery, aneurysms. 2) Acquired kidney disease ( diffuse glomerulonephritis, amyloidosis, Kimelstil-Wilson syndrome, systemic vasculitis, tumors). 3) Acquired lesions of the main renal artery (atherosclerosis, calcification, thrombosis, embolism, fibromuscular dysplasia, Takayasu's disease, aneurysm, endarteritis, hemangiomas, vascular compression, stenosis and thrombosis of the renal vein.
2. Arterial hypertension caused by damage to large vessels 1) Coarctation of the aorta 2) Atherosclerosis 3) Stenosis of the vertebral and carotid arteries 4) Complete AV blockade
3. Arterial hypertension in endocrine diseases 1) Pheochromocytoma 2) Itsenko-Cushing disease and syndrome 3) Primary hyperaldosteronism 4) Toxic goiter 5) Congenital adrenal hyperplasia 6) Acromegaly 7) Hyperparathyroidism
4. Arterial hypertension in diseases of the central nervous system 1) Encephalitis 2) Poliomyelitis 3) Tumors and injuries of the brain
features of hypertension in CGN and kidney disease: > Young age of patients; > Lack of "vegetative neurosis"; > The course of the disease without crises; > Dependence of exacerbations on tonsillitis and SARS, and not on psycho-emotional factors; > Patients with renal hypertension do not feel their high blood pressure, in contrast to patients with EG, in which even a slight increase may be accompanied by an abundance of symptoms; > Edema occurs in 1/3 of patients with CGN, but may also occur in EG, especially in the volume-sodium-dependent variant.
laboratory and instrumental studies: > Presence of urinary syndrome; > During the period of exacerbation - the acceleration of ESR, the appearance of acute phase proteins, often anemia; > In the presence of chronic renal failure - a decrease in glomerular filtration, an increase in residual nitrogen and urea, creatinine; > In the fundus - hypertensive retinopathy, usually more pronounced than in EG, transudates in the fundus can be observed even with moderate hypertension; > Needle biopsy of the kidneys.
Vasorenal hypertension Causes of vasorenal hypertension: > In old age - atherosclerosis; > In the young - FMD, less often nonspecific aortoarteritis (Takayasu's disease); > Rare causes are hypoplasia, thrombosis, post-traumatic aneurysm.
General signs of vasorenal hypertension 1. Stably high nature of hypertension from the very beginning; 2. Preferential increase in DBP; 3. Systolic murmur over the projection area of the renal arteries (with unilateral lesion, the murmur is audible in 50-70% of patients, with bilateral - in almost all); 4. Resistance to conventional antihypertensive therapy; 5. Frequent malignant course of hypertension (with unilateral lesion in 30%, with bilateral 50-60%); 6. Concomitant lesions of other arterial systems; 7. Asymmetry of pulse and blood pressure.
Primary hyperaldosteronism (Conn's syndrome) Characteristic signs (four "G"): 1. Hypertension; 2. Hypokalemia (potassium below 3.0 mmol/l); 3. Hyperaldosteronism; 4. Hyporeninemia.
Primary hyperaldosteronism (Conn's syndrome) o Severe muscle weakness resembling myasthenia gravis; o Convulsive muscle twitching, parasthesia, numbness and flaccid paralysis type disorder, often with hanging head symptom; o Persistent hypertrophy of the left ventricle does not develop, P-Q is shortened, electrical systole is lengthened, the ST segment is shifted down, the T wave is flattened and merges with a significantly enlarged U wave. o Polyuria (up to 3 l / day); o Nocturia; o Isosthenuria (1007-1015, and in diabetes insipidus 1002-1005).
Pheochromocytoma The main clinical manifestation of pheochromocytoma is a paroxysmal instantaneous increase in blood pressure to significant numbers (up to 250/140 - 300/160 mm Hg), accompanied by tachycardia up to 100-130 beats per minute, fever, dizziness, throbbing headache, trembling, pain in the epigastric region, limbs, pallor, increased respiration, dilated pupils, blurred vision, hearing, thirst, urge to urinate.
Pheochromocytoma In the blood and urine during an attack - leukocytosis, hyperglycemia, glucosuria; Urinary excretion per day more than 30 mcg of adrenaline, more than 100 mcg of noradrenaline and more than 6 mg of vanillindelic acid; CT - topical diagnostics.
Itsenko-Cushing's syndrome The disease occurs 3-4 times in women and in 80-90% of cases occurs with hypertension. In 30% of patients, the syndrome is due to primary adenoma or carcinoma of the adrenal cortex.
Itsenko-Cushing's syndrome Clinical symptoms: Obesity according to the "upper type": red and shiny face, powerful torso and neck and abdomen with thin legs; There are purple-violet striae on the abdomen and thighs, petechiae and telangiectasias are detected on the extensor surfaces of the forearms; Oligo- or amenorrhea, impotence and gynecomastia in men; Hair loss under the armpits, on the pubis, dry skin, nail dystrophy, acne; Acute steroid ulcers in the gastrointestinal tract, prone to bleeding; Insomnia, euphoria, fatigue and weakness;
Itsenko-Cushing's syndrome Laboratory data: polycythemia, eosinopenia, lymphopenia, hypercortisolemia, aldosteronemia, hypernatremia, hypomagnesemia, metabolic alkalosis, hypercholesterolemia, triglyceridemia, increased excretion of 17-OKS and 17-KS.
ISAH: isolated systolic hypertension o Increase in SBP above 140, with DBP below 90 mm. rt. Art. (high pulse pressure (“jumping” pulse, accent of 2 tones over the aorta, rough systolic murmur, conducted into the interscapular space. Aortic seal can be established using X-ray and Echo. KG examination.
Coarctation of the aorta Narrowing or complete break in the isthmus at the border of the arch and the descending aorta. It can be isolated, and can also be combined with patent ductus arteriosus or other congenital heart defects. It is 4 times more common in men.
Coarctation of the aorta When examining adult patients, good development chest, shoulder girdle and neck with a noticeable lag in the development of the lower extremities. The pulsation of the intercostal arteries is determined, the apex beat is strengthened, systolic trembling is often palpated in the 2-3 intercostal spaces to the left of the sternum. A systolic murmur is heard over the entire surface of the heart, which is carried out to the vessels of the neck and into the interscapular space. II tone on the aorta is accentuated. Systolic blood pressure in the upper extremities in all patients is significantly increased, while diastolic blood pressure rises slightly or remains normal. As a result, the pulse pressure increased. Blood pressure in the lower extremities is much lower than in the upper ones.
Coarctation of the aorta On the ECG in adults, signs of hypertrophy and overload of the left sections are revealed, in 70% of the plain chest radiographs, usuration of the ribs arising from the pressure of the intercostal arteries is determined. 2D echocardiography visualizes the site of narrowing of the aorta. Using Doppler echocardiography, systolic turbulent blood flow and pressure gradient above and below coarctation can be determined. The final diagnosis is made using aortography.
Target organ damage Heart left ventricular hypertrophy (LVH) heart failure Brain acute cerebrovascular accident (stroke, transient ischemic attack); chronic disorders of cerebral circulation (hypertensive encephalopathy, lacunar infarcts) Kidneys Hypertensive nephropathy Hypertensive nephrosclerosis Eyes Hypertensive retinopathy
Target organ damage Effects on the heart Left ventricular hypertrophy (LVH) Heart failure
Damage to target organs Effect on the brain acute cerebrovascular accident (stroke, transient ischemic attack); chronic disorders of cerebral circulation (hypertensive encephalopathy, lacunar infarcts)
Laboratory and instrumental research methods Complete blood count Complete urinalysis Biochemical blood test (levels of potassium, sodium, creatinine, glucose, cholesterol) ECG - left ventricular hypertrophy (Sokolov-Lyon index SV 1 + RV 5, 6> 35 mm in people older than 40 years; >> 45 mm in persons under 40 years of age) 24-hour monitoring of blood pressure (ABPM) Echocardiography - left ventricular hypertrophy (TZSLV >> 1.2 cm; TMZHP >> 1.2 cm; increased LVML), impaired diastolic, late systolic function of the left ventricle Fundus examination Ultrasound of the kidneys, adrenal glands, renal arteries to detect secondary hypertension
The location of the moment vectors of ventricular depolarization in the horizontal plane in the norm (a) and with LV hypertrophy (b) ECG with left ventricular hypertrophy
Treatment of hypertension Non-drug measures to reduce blood pressure Stop smoking Reduce excess body weight Reduce alcohol consumption Limit the intake of salt to 5-2 g / day Complex diet modification - increase the consumption of fruits and vegetables, foods rich in potassium, magnesium, calcium, fish and seafood, restriction of animal fats Increased physical activity
Drug treatment of hypertension 2. Main groups of antihypertensive drugs β-blockers Diuretics Calcium antagonists ACE inhibitors α-blockers of angiotensin receptors III drugs of central action
Group of drugs Representatives Indications Contraindications Diuretics Hypothiazid 12.5-50 mgmg Indapamide 1.25-2.5 mg Furosemide 40-240 mg Spironol kton 25-100 mg CHF, elderly age, systolic AH Gout
Group of drugs Representatives Indications Contraindications β-adrenergic blockers Propranolol 40-240 mgmg Atenolol 50-100 mg Metoprolol 50-400 mg Bisoprolol 2, 5-20 mg Angina pectoris, myocardial infarction, tachyarrhythmia syndrome m, m, AV block adade 2-3 degree
Group of drugs Representatives Indications Contraindications Calcium antagonists Verapamil 120-480 mg Diltiazem 180-360 mg Amlodipine 5-10 mg Nifedipine SRSR 30 mg diltia zema)
Group of drugs Representatives Indications Contraindications ACE inhibitors Captopril 25 mg, Enap (5, 10 mg), Diroton (10 mg) Arterial hypertension, chronic heart failure Pregnancy, bilateral renal artery stenosis, hyperkalemia
Group of drugs Representatives Indications Contraindications Angiotensin IIII receptor blockers Losartan 25-50 mg Valsarta n 80-320 mgmg Cough while taking ACE inhibitors Pregnancy, bilateral renal artery stenosis, hyperkalemia
Group of drugs Representatives Indications Contraindications Centrally acting drugs Clonidine 0.2-0.8 mg Methyldopa 500 mg-2g Moxonidine n Broncho-obstructive syndrome, hypersymptomatic aticotonia Bradycardia, heart block, depression
Group of drugs Representatives Indications Contraindications α-adrenergic blockers Doxazosin 1-16 mg Prazosin 2, 5-20 mg
Medicines for the relief of hypertensive crisis drug at dose Special indications Furosemid 20-120 mg IV bolus Pulmonary edema, hypertensive encephalopathy Clonid inin (Clonidine) 0.075-0.150 mg IV slowly In the syndrome withdrawal of clonidine
Medicines for the relief of hypertensive crisis drug at dose Special indications Labeto Lol 20-80 mg IV bolus Stroke, dissecting aortic aneurysm Captopril 6, 25-50 mg orally, sublingually Nifedi pin 10-30 mg sublingually
Complications of hypertension: Myocardial infarction Stroke Renal failure Heart failure Hypertensive encephalopathy Retinopathy Dissecting aortic aneurysm
Arterial hypertension is a stable increase in systolic blood pressure up to 140 mm Hg. and above and / or diastolic blood pressure up to 90 mm Hg. and above, according to 2 or more consecutive visits of the patient with an interval of at least 1 week.
CLASSIFICATION OF ARTERIAL HYPERTENSION Arterial hypertension Primary hypertension (essential hypertension, or hypertension) is a chronic disease of unknown etiology with a hereditary predisposition, as a result of the interaction of genetic factors, the external environment, characterized by a stable increase in blood pressure. Secondary hypertension (symptomatic) is based on any one, specific reason, the elimination of which is important not only to reduce or normalize blood pressure, but also to prevent complications.
ETIOLOGY Essential hypertension ETIOLOGY Essential hypertension Genetic predisposition Approximately 50% of patients have a hereditary predisposition to EG due to a mutation in the genes [mutation of angiotensinogen, angiotensin II receptors, angiotensin-converting enzyme, renin, aldosterone synthetase, β-subunit of sodium channels and amiloride sensitive other sodium
Other factors Obesity increases the risk of hypertension by five times. More than 85% of cases of hypertension occur in patients with a body mass index greater 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. table salt: excess sodium increases the volume of circulating blood, causes swelling of the walls of the carteriol, increases the sensitivity of the vascular wall to vasoconstrictive factors. carteriol Insufficient intake of calcium and magnesium, trace elements and vitamins with water and food. Alcohol abuse. Low physical activity, physical inactivity Psycho-emotional stressful situations.
The appearance of arterial hypertension depends on the age of the person. 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, kidneys. And after the age of 40, it is almost always the result of sclerotic vascular lesions. Pregnancy hypertension is hypertension that some women develop during pregnancy. It usually resolves after childbirth, but sometimes the disease can linger, and women who have had gestational hypertension, as well as preeclampsia and eclampsia, also accompanied by arterial hypertension, are more likely to develop hypertension in later years. occurs four times more often than whites, develops faster and leads to higher mortality, prevalence, but not severity, of essential hypertension in them decreases with a decrease in overt or covert racism
CLASSIFICATION CLASSIFICATION (by degree) OF ARTERIAL HYPERTENSION BY THE LEVEL OF BP (according to experts from WHO and MLG, 1999) 
By stage Hypertension stage I implies the absence of changes in the target organs. Stage II hypertension is characterized by the presence of one or more changes in the target organs. Stage III hypertension is established in the presence of one or more associated (comorbid) conditions.
55 years old women > 65 years old Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg %) Diabetes mellitus Men > 55 years Women > 65 years Smoking Total blood cholesterol > 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 > 6.5 mmol / l (250 mg %) Diabetes mellitus Familial cases of early development of hypertension, cardiovascular disease 55 years old women > 65 years old Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetic mellitus "> 55 years old women > 65 years old Smoking Total blood cholesterol level > 6.5 mmol/l (250 mg%) Diabetes mellitus Familial cases early development of hypertension, cardiovascular diseases"> 55 years old women > 65 years old Smoking Total blood cholesterol > 6.5 mmol / l (250 mg %) Diabetes mellitus" title="(!LANG: Risk factors Used for risk stratification diastolic blood pressure (grade 1-3) Age men > 55 years women > 65 years Smoking Total blood cholesterol > 6.5 mmol/l (250 mg%) Diabetes mellitus"> title="Risk factors Used for risk stratification Systolic and diastolic blood pressure (grade 1-3) Age men > 55 years women > 65 years Smoking Total blood cholesterol > 6.5 mmol/l (250 mg%) Diabetes mellitus"> !}
Other factors Smoking Excess consumption of table salt Salt Insufficient intake of water and food calcium and magnesium, trace elements and vitamins.calcium magnesium Alcohol abuse. Low physical activity, physical inactivity. Physical inactivity Psycho-emotional stressful situations. Reduced HDL cholesterol Elevated LDL cholesterol Microalbuminuria (mg/day) in diabetes mellitus Impaired glucose tolerance Elevated blood fibrinogen High-risk socioeconomic groups
300 mg/day) and/or a slight increase in plasma creatinine (1.2-2 mg/dl) or microalbuminuria Proteinuria creatinine microalbuminuria Feature" title="(!LANG: Target Organ Damage Left Ventricular Hypertrophy Left Ventricular Hypertrophy Proteinuria (>300 mg/ days) 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 slight increase in plasma creatinine (1.2–2 mg/dL) or microalbuminuria Prote Generalized or focal narrowing of the retinal carteria 300 mg/day) and/or slight increase in plasma creatinine (1.2-2 mg/dl) or microalbuminuria dl) or microalbuminuria ProteSigns of atherosclerotic lesions of the carotid, iliac and femoral carteries, aorta Atherosclerotic Generalized or focal narrowing of the retinal carteries "> 300 mg / day) and / or a slight increase in plasma creatinine concentration (1.2-2 mg / dl) or microalbuminuria ProteinuriacreatinineMicroalbuminuria Feature" title="(!LANG:Target Organ Damage Left Ventricular Hypertrophy Left Ventricular Hypertrophy Proteinuria (>300 mg/day) and/or slight increase in plasma creatinine (1.2-2 mg/dL) or microalbuminuria ProteFeature"> title="Target organ damage Left ventricular hypertrophy Left ventricular hypertrophy Proteinuria (>300 mg/day) and/or slight increase in plasma creatinine (1.2–2 mg/dL) or microalbuminuria ProteSign"> !}
Concomitant clinical conditions Ischemic stroke Hemorrhagic stroke Transient cerebrovascular accident Myocardial infarction Angina pectoris Revascularization of the coronary arteries Congestive heart failure Heart failure Diabetic nephropathy Renal failure (creatinine in blood plasma above 2 mg/dL) Dissecting aneurysm Severe hypertensive retinopathy Hemorrhages or exudates Hemorrhages of the optic tract Edema nerve
Pathogenesis of Essential AH BUT! Subcortical structures A! pressor centers of the medulla oblongata and nucleus of the hypothalamus A! Sympathoadrenal s-we A! humoral pressor systems: ADH, synthesis of releasing factors ACTH, TSH Distribution of the peripheral crankcase. Spasm through the sympathoadrenal system Kidney ischemia A! YUGA and A! RAAS Total peripheral resistance to blood flow (sympathetic ADH, ACTH) A! SAS and RAAS Vessel remodeling. 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, endcarteritis, thrombosis, embolism, renal aneurysm, vein stenosis and thrombosis, renal vascular injury); anomalies of the kidneys and urinary system (polycystic, hypoplasia); - secondary kidney damage in tuberculosis, diffuse diseases of the connected tissue (SLE, systemic scleroderma); 2) endocrine hypertension (pheochromocytoma; primary hyperaldosteronism (Cohn's syndrome); Cushing's disease (syndrome); hyperparathyroidism; acromegaly; climacteric hypertension; 3) hemodynamic hypertension (atherosclerosis of the aorta; stenosis of the carotid and vertebrobasilar arteries; coarctation of the aorta; aortic insufficiency; rheological hypertension polycythemia vera); 4) neurogenic hypertension (vascular diseases and brain tumor; inflammatory diseases - encephalitis, meningitis, poliomyelitis; brain injury; polyneuritis. 5) special forms of symptomatic drug hypertension (anabolic steroids and mineralocorticoids, oral contraceptives containing progesterone and estrogens, sympathomimetics, indomethacin and others).
Renal arterial hypertension Renovascular arterial hypertension Renovascular (renovascular) hypertension (RVAH) is a persistent increase in arterial pressure caused by impaired circulation of one or both kidneys as a result of insufficient blood supply. CAUSES Congenital: - fibromuscular dysplasia of the renal carteria; - anomalies in the development of the aorta; - compression of the renal carteria Acquired: - atherosclerotic process; -thrombosis; - renal embolism; - pankarteritis; --nephroptosis
RENAL ISCHEMIA A! YUGA A! ejection of RENINA + A! RASS formation of ANGIOTENSIN II Stimulation of the glomerular zone of the adrenal cortex Release of ALDOSTERONE Retention of Na Retention of H2O in the dist. parts of the nephron BP Secretion of ADH + delay H2O BCC Powerful vasoconstrictor OPSS BP Acts on the HYPOTHALAMUS and increases 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, there are high numbers of blood pressure that are resistant to therapy. - As a rule, there are no hypertensive crises. - Primary increase in DBP, pulse BP is reduced. - Tendency to orthostatic hypotension. - Vascular systolic murmur or systolic-diastolic murmur in the umbilical region (in the projection of the renal cartery from the aorta). - Transient or persistent signs of impaired renal function.
Renoprival arterial hypertension Damage to the renal glomeruli Damage to the renal parenchyma: glomerulonephritis, systemic scleroderma, systemic lupus erythematosus, amyloidosis Diabetic nephropathy DISTURBANCE OF VASODILATOR V-B IN THE KIDNEYS: Bradykinin Prostaglandins Impairment of the ability of the kidneys to inactivate vasopressor substances In case of damage to the glomeruli, impaired fluid excretion - increase in BCC - increase in blood pressure
CLINIC GLOMERULONEPHRITIS - Young age. - Primary increase in DBP, with SBP not exceeding 180 mm Hg. - BP stability. - Absence of crises. The presence of at least minimal changes in the study of urine, with a predominance of erythrocytes and cylinders. The diagnosis is established on the basis of a Doppler study and X-ray methods of investigation, but the final one is only on the basis of a biopsy.
Chronic pyelonephritis This determines the clinical signs of the underlying disease: chilling, dysuria, oliguria, puffiness of the face, subfebrile condition, signs of an inflammatory process in the blood and urine. But with a long history, hypertension becomes persistent, with a predominant increase in DBP. In the study of urine against the background of exacerbation of pyelonephritis, persistent hypoisostenuria, leukocyturia and bacteriuria are determined, sometimes hematuria. A urine culture is required. In the study of blood - clinical signs of inflammation, there may be anemia. The diagnosis is established on the basis of instrumental research methods - detection of deformation of the pelvicalyceal apparatus, reduction in the size of the kidneys and dysfunction, asymmetry of the lesion.
Polycystic Increased blood pressure in polycystic 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 a significant increase in the kidneys, the diagnosis can be suspected by palpation, and confirmed by 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 due to: 1) hyperproduction of cortisol with activation of the central nervous system, 2) increased sensitivity of blood vessels to the vasoconstrictor action of norepinephrine and other vasopressor agents, 3) retention of sodium and water by the kidneys with an increase in circulating blood volume, since hypercotrizolemia, as a rule, is combined with excessive formation of mineralocorticoids, 4) excessive formation of angiotensin II.
Arterial hypertension in hypercortisolism, as a rule, does not reach high numbers, is systolic-diastolic in nature, proceeds without crises and has a relatively benign course. But if untimely detected and untreated, it can lead to vascular complications and death.
Hyperaldosteronism Hormone producing a tumor of the glomerular zone 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 GM to catecholamines; HYPERTHYROISIS - OPSS; heart rate; UO HYPOTERIOSIS - myxedema - accumulation of acidic glycosaminoglycans - which I are sorbents of Na H2O + Comm. The tissue surrounding the neurovascular bundles compression of the peripheral vascular resistance + blood pressure and edema occurs
Hemodynamic arterial hypertension Hemodynamic arterial 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 in aortic coarctation; c) hyperkinetic hypertension in carteriovenous fistulas. Arterial hypertension as a result of aortic atherosclerosis is diagnosed on the basis of such signs: advanced age of the patient, accent of the second heart sound and a metallic shade over the aorta, systolic murmur over the aorta, increased systolic blood pressure, signs of atherosclerosis of the peripheral carteries, aorta dilatation according to x-ray and ultrasound.
Hemodynamic arterial hypertension Arterial hypertension in aortic regurgitation is characterized by an increase in systolic and a decrease in diastolic blood pressure high level pulse pressure. Arterial hypertension in coarctation of the aorta is manifested by an increase in blood pressure in the upper extremities and its decrease in the lower extremities. On palpation, an intense pulsation of the intercostal carteries is determined, a decrease in the pulsation of the peripheral carteries on the lower extremities, on auscultation - a coarse systolic murmur over the projection of the thoracic aorta along the anterior surface of the thoracic
Clinic of arterial hypertension COMPLAINTS OF THE PATIENT: 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 STUDY The general condition of the patient is satisfactory. With the progression of the disease and the appearance of complications, the general condition of the patient can be from moderate to severe (hypertensive crisis, acute and chronic heart failure, transient ischemic attacks). Skin color - hyperemia. Body weight: More often, patients are overweight or obese.
Diagnostic program of mandatory studies in the detection of hypertension Mandatory studies: - collection of complaints and anamnesis; - clinical examination; - measurement of blood pressure on both arms; - measurement of blood pressure on the lower extremities - measurement of body weight and waist circumference; - laboratory examination: general blood and urine tests, urinalysis according to Nechiporenko, 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 arterial 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 analysis of urine does not detect changes in the initial stages of the disease. With the development of hypertensive nephropathy, microalbuminuria is determined, later proteinuria. Microscopic examination of urine sediment: leukocytes, micro- and macrohematuria, granular casts. Biochemical blood test: hypercholesterolemia, hypertriglyceridemia, lowering high-density cholesterol. X-ray examination reveals left ventricular hypertrophy, atherosclerotic lesions of the aorta, venous congestion in the lungs. Electrocardiography: signs of left ventricular hypertrophy, left ventricular systolic overload, signs of coronary insufficiency, negative or biphasic T wave, S-T segment depression, signs of myocardial infarction, arrhythmia and cardiac conduction. Echocardiography: thickening of the interventricular septum, the posterior wall of the left ventricle, an increase in the mass of the myocardium and voids of the heart, a decrease in myocardial contractility according to the ejection fraction. When conducting Doppler echosonography, atherosclerotic lesions of the carotid carteries are detected. Examination of the fundus determines angiopathy of the retina, mainly capillaries, but damage to larger vessels is possible - carteria. At the same time, pathological changes occur in venous vessels.
Electrocardiography in hypertension 1. left ventricular systolic overload, 2. sign of left ventricular hypertrophy, 3. sign of coronary insufficiency, 4. negative or biphasic T wave, 5. S-T segment depression, 6. sign of previous myocardial infarction, 7. rhythm and conduction disturbance hearts.
How to treat hypertension? The therapy is aimed at solving the following problems: Achievement of the target pressure level. It should be no more than 140/90. For elderly patients with severe hypertension, a decrease in systolic pressure to 160 mm Hg is recommended. Art. Correction of modifiable risk factors. Prevention and treatment of associated pathologies. One of the main therapeutic agents is lifestyle modification.
Weight loss. Weight loss for every 10 kg can reduce pressure by up to 20 mm Hg. Art. Limiting the consumption of table salt (recommended no more than 5 g per day). It has been found that in cultures where salt intake is traditionally high, 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. Enough half an hour classes 4 times a week. Refusal of alcohol. It is allowed to take 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 mm Hg. Art. Diet therapy. It is recommended to increase the consumption of foods rich in dietary fiber, potassium, calcium, magnesium. You need to reduce your fat intake. The effectiveness of the means of reducing pressure by 8-14 mm Hg. Art. Increasing resistance to psycho-emotional stress (mastering the techniques of psychological self-regulation).
The main groups of drugs Diuretics Diuretics To combat hypertension with preserved kidney 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 practically does not affect metabolic processes. Diuretics can be used as monotherapy or in combination with other antihypertensive drugs. A feature of modern diuretics is to reduce the risk of addiction. Thiazide-like diuretics are the drugs of choice for heart failure in the older age group, as well as in patients with osteoporosis and coronary artery disease. Furosemide and other loop diuretics are not used to treat hypertension due to their low antihypertensive efficacy and high frequency of side effects. The use of this group becomes necessary only with a pronounced decrease in the function of the heart and kidneys treatment of hypertension
Calcium antagonists, representatives of this group are derivatives of nifedipine, verapamil and diltiazem. More recently, taking "nifedipine 10 mg sublingually" was the standard of care for emergency care in hypertensive crisis. Now this method of pressure reduction 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 should not be used immediately after myocardial infarction and patients suffering from heart failure. Verapamil and diltiazem, in addition to affecting blood pressure, are successfully used to treat angina pectoris and arrhythmias.
ACE inhibitors A group that includes drugs 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 correct the negative consequences of its long 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 disease. 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 inhibit the formation of the hormone angiotensin II, the activity of which is especially high in kidney damage, thereby preventing their damage. In addition, ACE inhibitors actively inhibit pathological changes that occur through the fault of the same angiotensin II in the heart and blood vessels. ACE inhibitors are especially indicated in cases of concomitant heart failure without symptoms of left ventricular dysfunction, diabetes mellitus, myocardial infarction, non-diabetic nephropathy, microalbuminuria and metabolic syndrome
Sartans (Angiotensin Receptor Blockers) Closely related to the ACE inhibitor group, sartans have similar mechanisms of action. But in contrast to ACE inhibitors, the use of sartans by patients with hypertension is better tolerated - they rarely 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 in case of similar indications, but with poor tolerance to ACE inhibitors
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 paramount importance for the treatment of hypertension. The appointment of beta-blockers is especially appropriate for the combination of hypertension with coronary artery disease, heart failure, hyperthyroidism, arrhythmias and glaucoma. It 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 not possible 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 when hypertension is combined with prostatic hypertrophy. In cardiology, alpha-blockers are used to treat Prinzmetal's angina (prazosin) and symptomatic therapy 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 hypotension of the first dose and orthostatic hypotension, which the doctor usually warns the patient about. To achieve target blood pressure figures, 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 (Dopegyt), guanfacine (Estulik) and clonidine (Clonidine), while 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 pregnancy. Compared with 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 the target figures for blood pressure, 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 proven to be effective in lowering blood pressure and reducing proteinuria, but so far its positive effect on cardiovascular morbidity and mortality has not been proven due to the relatively short period of its existence. Several studies are currently underway on this drug. Direct vasodilators (hydralazine, minoxidil) are currently used extremely rarely.
