Presentation on essential hypertension. Presentation on the topic “Arterial hypertension. Non-drug methods for the treatment of hypertension

Slide 1

Essential hypertension and its complications from the point of view of a general practitioner

Scientific adviser: I.N. Bobrovsky Compiled by: Yu.N. Fefelova, I.A. Cherkasov, O.R. Hasanli

State Educational Institution of Higher Professional Education Stavropol State Medical Academy of the Ministry of Health and Social Development of Russia Department of Public Health, Healthcare Management, Economics and Social Work

Slide 2

Hypertension is a disease, the main symptom of which is an increase in blood pressure caused by a violation of the regulation of vascular tone and heart function. There are two types of this disease: -primary -secondary Primary essential or arterial hypertension is called an increase in blood pressure only in hypertension. Secondary arterial hypertension is often a symptom of latent inflammation of the kidneys or damage to the renal vessels.

Slide 3

The main complications that arise in hypertension: -Brain stroke -Myocardial infarction -Ischemic heart disease -Stenocardia -Arrhythmia -Arterial hypertension -Hypertensive crisis -Aterosclerosis -Atrioventricular blockade -Heart failure -Spinal stroke

Slide 4

The main risk factors are: -high level of cholesterol in the blood -obesity -smoking -degree of high blood pressure -stress -imbalance -alcohol-diabetes mellitus -overweight -harmful production factors

Slide 5

The first symptoms: - weakness - headache - fatigue - sleep disturbance

Symptoms of complications: - dizziness - nausea - vomiting - heart pain - shortness of breath

Slide 6

Stages of the disease, symptoms During hypertension, three stages are distinguished: I - stage of functional changes. During this period, patients are worried about weakness, headache, fatigue, sleep disturbances. High blood pressure is not constant, it normalizes under the influence of rest and sedatives. No changes in internal organs were found. II - stage of initial organic changes. Blood pressure is increased, to reduce it requires the use of special hypothetical drugs. Hypertensive crises may occur. The course of atherosclerosis, ischemic heart disease is aggravated, damage to the kidneys, eyes and other organs appears. The left ventricle of the heart is enlarged. III - stage of pronounced organic changes. Blood pressure is steadily increased. Complications can occur, such as myocardial infarction, cerebral stroke, heart failure, blindness.

Slide 7

Diagnostics: -collection of anamnesis -objective research -laboratory and instrumental studiesTreatment is based on various methods: -medication -surgical

Classification of blood pressure levels (WHO, MTF, 1999)
Optimal blood pressure
.
< 120
< 80
Normal blood pressure
< 130
< 85
Increased
normal blood pressure
130-139
85-89
Degree 1
140-159
90-99
Degree 2
160-179
100-109
Degree 3
> 180
> 110
Isolated
systolic
> 140
< 90

Primary - essential hypertension - 85-90% (after excluding secondary hypertension) Secondary or symptomatic hypertension - 5-23%

Arterial hypertension (essential or
primary) - a disease characterized by
raising
HELL,
conditioned
sum
genetic and external factors and unrelated
with any independent lesions
organs and systems (the so-called secondary
hypertension,
at
which
arterial
hypertension is one of the manifestations
diseases).

Risk factors for hypertension
Genetic
Overweight
Metabolic syndrome
(insulin resistance syndrome)
Alcohol abuse
Cooking abuse
salt
Psychosocial stress

Etiology The neurogenic theory put forward by G.F. Lang, where the leading link in pathogenesis is a violation of higher nervous activity, fuss

Etiology
The neurogenic theory put forward by G.F. Lang,
where the leading link in pathogenesis is
violation of the highest nervous activity,
stimulated
external environment and leading to persistent
excitement
vegetative
centers
regulation
blood circulation,
a
also
increase in blood pressure.

Pathogenesis

EAH main causative factor - increased activity
sympathoadrenal nervous system
Vasospasm (renal arteries)
Stimulation of the South
RENIN protease
Conversion of ANGIOTENSIN 1 into
ANGIOTENSIN 11
increased blood pressure due to NaCl hypervolemia

The defeat of target organs in hypertension:

Heart
angina
myocardial infarction
heart failure
Brain
hypertensive
encephalopathy, transient ischemic
attacks, stroke, vascular dementia
Ophthalmic
bottom
Kidney
edema
exudation
hemorrhage
nephropathy
renal failure
Vessels
occlusive lesions
peripheral arteries
dissecting aortic aneurysm

CLINICAL PICTURE
Main complaints:
headaches, especially in the morning, are in the nature of migraines,
come in the form of an attack, last for many hours, end
often vomiting. Localization of pain: occipital region, parietal, frontal,
temporal, in the area of ​​the eyeballs, the lower part of the forehead, etc.
dizziness and tinnitus. Dizziness depends on tone disturbance
vessels and circulatory disorders in the brain, are replaced by the appearance
short-term loss of consciousness (transient ischemic attacks), and then
ischemic and hemorrhagic strokes.
Functional noises are never permanent. Noises caused by
atherosclerotic lesions of the cerebral vessels are permanent
character.
Astheno-neurotic: fatigue, insomnia, increased
excitability, palpitations, prolonged pain in the region of the heart (apex),
inability to sleep on the left side, etc. There may be complaints of numbness,
"Creeping creeps" and cold extremities.
"Nocturia" - the predominant excretion of urine at night, with
progression - oliguria is detected (a decrease in the daily amount
excreted urine), up to anuria (complete cessation of urine excretion), which
indicates the formation of a shriveled kidney and renal failure.
the appearance of "shiny stars", "flying flies" associated with
vasoconstriction of the fundus, then vasoconstriction becomes persistent
character, which leads to decreased vision.

Diagnostic tests Physical examination

Visually
Signs of "metabolic obesity" of the android type,
correlating with:
insulin resistance,
hyperinmulinemia,
hyperglycemia
violation of fat metabolism
high blood pressure
Palpation
Pulse on the radial artery is tense
The apical impulse is reinforced, ascending
Pulsation of the dilated aorta in the jugular fossa
Percussion
With the development of heart failure, the expansion of boundaries
hearts first to the left and then to the right
Auscultation
Accent 11 tones above the aorta, sometimes diastolic murmur.
Systolic murmur above the apex (1 point of auscultation).
The appearance of the gallop rhythm, additional tones - functional
myocardial insufficiency.

Laboratory research

General analysis urine - low specific gravity,
proteinuria
Biochemical blood test - content
sugar, urea, creatinine, electrolytes
Urine analysis according to Zimnitsky - for
objectification of anamnestic indications of
nocturia, oliguria, hypoisostenuria.
Rehberg's test - to identify signs
renal failure.

Instrumental research methods

ECG - revealing signs of myocardial hypertrophy,
ischemic
changes
at
joining
Ischemic heart disease,
identification of rhythm disturbances.
On
Echocardiography
for
identifying
hypertensive
remodeling of the myocardium.
Ultrasound of the kidneys and adrenal glands - to look for signs
wrinkling of the kidneys, adrenal adenoma.
Examination of the fundus - narrowing of the retinal arteries. Veins
expanded, sometimes "corkscrew" crimped.
With the development of atherosclerosis, arteriovenous impressions
Samosa-Guna.
X-ray angiographic studies - with vasorenal
AH of various etiology and coarctation of the aorta.
X-ray, MRI
skull - if you suspect
endocrine hypertension.

Classification and stratification of hypertension

HELL LEVEL
1st level
GARDEN 140 - 159 mm s.b.
DBP 90 - 99 mm s.b.
2nd level
GARDEN 160 - 179 mm s.b.
DBP 100 - 109 mm s.b.
Level 3
GARDEN> 180 mm s.b.
DBP> 110 mm s.b
CATEGORY
RISK FACTOR
Risk factor 1
(low risk)
Risk factor 2
(medium risk)
Risk factor 3
(high risk)
1-3 level
Risk factor 4
(very tall
risk)
DIAGNOSTIC CRITERIA
Absent
risk factors for hypertension
target organ damage,

associated diseases
Present
1 or more risk factors for hypertension,
signs of target organ damage,
Present
risk factors for hypertension
target organ damage
complications of the cardiovascular system
associated diseases
Present
risk factors for hypertension
target organ damage
complications of the cardiovascular system
associated diseases
diabetes

PRINCIPLES OF TREATMENT OF ARTERIAL HYPERTENSION
NON-MEDICINAL
Combating Modifiable Risk Factors:
smoking
obese
alcohol abuse
with violations of the regime of work and rest (stress)
hypodynamia
limiting the intake of table salt
MEDICAMENTAL
The main antihypertensive drugs:
Diuretics
Β-blockers
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin II receptor blockers
Slow calcium channel blockers
Centrally acting drugs
Α1-adrenergic receptor blockers

Diuretics
Thiazide or similar compounds (hypothiazide, indapamide
(arifon), chlorthalidone, brinaldix, etc.)
Loop diuretics (furosemide, uregit, burinex, etc.)
Application and dosage regimen
The initial daily dose (12.5 mg) of hypothiazide with
the need is increased to the maximum (50 mg).
Hypothiazide diuretics are ineffective in reducing clearance
creatinine less than 35 ml / min and a decrease in the glomerular
filtration less than 25 ml / min. In such a situation, they switch to
furosemide 40 mg x 1 time per day, 1-2 times a week.
Indapamide 2.5 x 1 times a day daily, in comparison with others
diuretics have a number of advantages: it does not cause disturbances
glucose tolerance, with prolonged use reduces
left ventricular hypertrophy, effective in chronic
renal failure

Β-blockers
Mechanism of action in hypertension:
decrease in heart rate (reduces the frequency and strength of heart contractions);
reduces the secretion of renin;
reduces sympathetic activity;
increases the level of prostaglandins in the vascular wall
increases the sensitivity of baroreceptors.
Subdivided into:
Non-selective (propranolol, sotalol, pindolol, nadolol, etc.)
Selective β-metoprolols (atenolol, egilok), bisaprolol
(concor), etc.
With internal sympathomimetic activity (whiskey,
acebutalol, oxprenolol, etc.)
α-β-blockers (labetalol, carvedilol, etc.)

Angiotensin-converting inhibitors
enzyme (ACE inhibitors)
These drugs suppress the transformation of AT-I into AT-II.
renin rises
a
the level of AT-II and aldesterone decreases.
The antihypertensive effect of ACE inhibitors is associated with
dilatation of peripheral arterioles.
An important secondary mechanism is associated with an increase in
the content of the hypotensive fraction of prostaglandins.
ACE inhibitors
have nephroprotective
action,
due to
what
declines
intraglomerular hypertension and proteinuria, which
important for patients with diabetes mellitus.

Certain ACE inhibitors. Frequency of use, daily doses, onset of the antihypertensive effect and its duration

Average doses
(mg)
Frequency
application
(once a day)
50-100
2-3
4-6
1
Fozinopril (monopril)
10-40
1-2
Enalapril (Renitek)
10-20
1-2
A drug
Captopril (kapoten)
Perindopril (prestarium)

Angiotensin 11 receptor blockers

have a double mechanism of action,
blocking:
action of norepinephrine
α1-adrenergic receptors at the level
synaptic cleft
it
accompanied by
practical
lack of
collateral
effects.
The representative of eprosartans is
Teveten 600 mg x 1 time per day,
losartanov - Lozap 25-50 mgx2 times a day

Slow calcium channel blockers

The mechanism of action of calcium antagonists is
inhibition of the entry of Ca ++ ions into the myocytes of vascular
walls, which causes them to relax and, as a result,
dilatation.
Calcium antagonists are composed of various chemical
connections:
phenylalkylamines (verapamil, isoptin, etc.);
benzodiazepines (diltiazem, cardil, etc.);
dihydropyridines (corinfar, isradipine, amlodipine,
nitrendipine, felodipine, etc.).
Dihydroperidines have the most vasodilatory effect
expressed.

Α1-adrenergic receptor blockers

Prazosin, doxazosin, etc.
These are indirect vasodilators, mechanism of action
which
consists
v
blockade
postsynaptic
α1-adrenergic receptors,
decrease in total peripheral vascular
resistance,
not
causing
at
this
reflex tachycardia.
Treatment begins with small doses (1 mg / day), in
the subsequent dosage is gradually increased
up to 10 mg / day.

Centrally acting drugs

The result of central stimulation of α2-adrenergic receptors and β1imidazoline receptors:
decreased secretion of catecholamines by chromaffin cells
adrenal glands;
decreased activity of the sympathetic nervous system;
increased tone of the vagal nerve.
The above effects reduce the total peripheral
vascular resistance, heart rate and strength.
Central α2-adrenergic agonists - clonidine 0.0075-0.015 mg, etc.
Central α-agonists reduce sympathetic activity.
Side effect - dry mouth, drowsiness.
Representatives of the new
class - agonists of central imidazoline receptors
(moxonidine in the form of zinc preparations, physiotens 0.2-0.4 mg x 1 time
day, etc.).

Clinic features

Debut of the disease under 20 years of age and over 60 years
Suddenly persistent and very high,
predominantly DBP (> 110 mm Hg),
malignant course
The presence of crises with the clinic of sympatho-adrenal
excitement
Lack of genetic predisposition
or indications of kidney disease
Resistance to drug therapy

Kidney disease

Parenchymal
(glomerulonephritis, nephritis)
Chronic pyelonephritis
Polycystic kidney disease
Diabetic nephropathy
Hydronephrosis
Congenital renal hypoplasia
Traumatic kidney injury
Renovascular hypertension

Renovascular hypertension (RVH) is an increase in blood pressure due to narrowing of the renal artery or its branches.

Renovascular
th hypertension
(RVG) -
increase in blood pressure,
conditioned
constriction
renal
artery or her
branches.

Renovascular hypertension

Coarctation of the aorta

Endocrine diseases

Acromegaly (pituitary gland)
Hypothyroidism
Hyperthyroidism
thyroid
Hypercalcemia
Adrenal adenomas
- Cushing's syndrome,
- primary aldosteronism or
Cohn's syndrome
- pheochromacytoma

Acromegaly

Neurological diseases

Intracranial hypertension
Brain tumor
Encephalitis
Sleep apnea
Tetraparesis
Acute porphyria
Guillain-Barré syndrome


































































1 in 65

Presentation on the topic: Arterial hypertension

Slide No. 1

Slide Description:

Slide No. 2

Slide Description:

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

Slide No. 3

Slide Description:

Distinguish between essential (primary) and secondary arterial hypertension. Essential arterial hypertension is 90-92%, secondary - about 8-10% of all cases of high blood pressure. Distinguish between essential (primary) and secondary arterial hypertension. Essential arterial hypertension is 90-92%, secondary - about 8-10% of all cases of high blood pressure.

Slide No. 4

Slide Description:

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

Slide No. 5

Slide Description:

Slide No. 6

Slide Description:

if the levels of systolic and diastolic blood pressure fall into different classification categories, then it is necessary to select more high category... if systolic and diastolic blood pressure levels fall into different classification categories, then the higher category should be selected. As a criterion for the diagnosis of hypertension, the levels of systolic and diastolic blood pressure should be used equally; to determine the degree of isolated systolic hypertension, the gradations given in the column "systolic blood pressure" are used.

Slide No. 7

Slide Description:

Experts from WHO and MOGA proposed risk stratification into four categories (low, medium, high and very high) or risk 1, 2, 3, 4. Experts from WHO and MOGA 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 data on the probability of death from cardiovascular diseases, as well as from myocardial infarction and stroke. To determine the individual patient's degree of risk of developing cardiovascular complications, 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.

Slide No. 8

Slide Description:

Risk factors for cardiovascular diseases Risk factors for cardiovascular diseases 1. Used for risk stratification The value of systolic and diastolic blood pressure Age: men over 55 women over 65 years Smoking Total cholesterol levels over 6.5 mmol / l Diabetes mellitus Familial cases of early development SS diseases

Slide No. 9

Slide Description:

2. Other factors adversely affecting the prognosis 2. Other factors adversely affecting the prognosis Reduced HDL cholesterol Elevated LDL cholesterol Microalbuminuria (30-300 mg / day) with diabetes Impaired glucose tolerance Obesity Sedentary lifestyle Increased blood fibrinogen levels Social high-risk economic groups

Slide No. 10

Slide Description:

Damage to target organs Damage to target organs Left ventricular hypertrophy (ECG, Echo-CG, Rtg) Proteinuria and / or a slight increase in plasma creatinine concentration Ultrasound or radiological signs of atherosclerotic lesions of the carotid, iliac and femoral arteries, aorta Generalized or focal narrowing of the retinal arteries

Slide No. 11

Slide Description:

Associated clinical conditions Associated clinical conditions Cerebrovascular diseases: Ischemic stroke Hemorrhagic stroke: Transient ischemic attacks Heart disease: MI Angina pectoris Revascularization of coronary arteries Congestive heart failure Renal disease: Diabetic nephropathy Renal failure Vascular diseases: Dissection of peripheral arteries exudates Edema of the optic nipple

Slide No. 12

Slide Description:

Slide No. 13

Slide Description:

Slide No. 14

Slide Description:

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

Slide No. 15

Slide Description:

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

Slide No. 16

Slide Description:

this is an increase in blood pressure, etiologically associated with certain, usually clinically well-defined diseases of organs and systems involved in the regulation of blood pressure. this is an increase in blood pressure, etiologically associated with certain, usually clinically well-defined diseases of organs and systems involved in the regulation of blood pressure.

Slide No. 17

Slide Description:

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 nephrosistosis Diabetic lesions of the kidneys Diabetic nephrosis Goodpasture

Slide No. 18

Slide Description:

1.2 Renovascular hypertension 1.2 Renovascular hypertension Renal arterial atherosclerosis Fibromuscular hyperplasia of the renal arteries Renal artery and venous thrombosis Renal artery aneurysms Nonspecific aortoarteritis 1.3 Renin-producing renal tumors 1.4 Primary renal sodium retention syndrome

Slide No. 19

Slide Description:

2. Endocrine 2. Endocrine Adrenal (sm Itsenko-Cushinga, congenital virilizing hyperplasia of the adrenal cortex, primary hyperaldosteronism, pheochromocytoma) Hypothyroidism Acromegaly Hyperparathyroidism Carcinoid 3. Pregnancy of the aorta 4.

Slide No. 20

Slide Description:

5. Neurological disorders 5. Neurological disorders Increased intracranial pressure (brain tumor, encephalitis, respiratory acidosis) Quadriplegia Lead intoxication Acute porphyria Hypotalpmic (diencephalic) sm Family disautonomy S. Guillain-Barré Sleep apnea of ​​central genesis

Slide No. 21

Slide Description:

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

Slide No. 22

Slide Description:

7. Drug-induced hypertension, as well as exogenous intoxication Taking oral contraceptives 7. Drug-induced hypertension and exogenous intoxication Taking oral contraceptives Treatment with corticosteroids, mineralocorticoids, sympathomimetics, estrogens Treatment with monoamine oxidase inhibitors, simultaneously with ingestion of pigs, , thallium, cadmium 8. Increased BCC Excessive intravenous infusion Polycythemia vera 9. Alcohol abuse (chronic alcoholism)

Slide No. 23

Slide Description:

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

Slide No. 24

Slide Description:

Arterial hypertension 1 tbsp. Risk 2. Dyslipidemia. Arterial hypertension 1 tbsp. Risk 2. Dyslipidemia. AG 2 tbsp. Risk 3. Hypertensive heart H1. Ventricular premature beats. AG 2 tbsp. Risk 4. Diabetes mellitus, 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. H 1. Polycystic kidney disease. Chr. pyelonephritis, without exacerbation. Secondary nephrogenic hypertension.

Slide No. 25

Slide Description:

After establishing the diagnosis of hypertension and assessing the cardiovascular risk, an individual tactics of patient management is developed. After establishing the diagnosis of hypertension and assessing the cardiovascular risk, an individual tactics of patient management is developed. Important aspects of managing a patient with hypertension are: Motivation of the patient for treatment and adherence to recommendations for changing lifestyle and drug therapy regimen. The experience and knowledge of the doctor and the patient's trust in him. Decision on the appropriateness and choice of drug therapy.

Slide No. 26

Slide Description:

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

Slide No. 27

Slide Description:

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

Slide No. 28

Slide Description:

to carefully identify the patient's complaints indicating damage to target organs: to carefully identify the patient's complaints indicating damage to target organs: brain, eyes - the presence and nature of headache, dizziness, sensory and movement disorders, visual impairment; heart - chest pains, their connection with rises in blood pressure, emotional and physical stress, palpitations, interruptions in the work of the heart, shortness of breath; kidneys - thirst, polyuria, hematuria, nocturia; peripheral arteries - cold extremities, intermittent claudication. to assess the possible impact on the hypertension of environmental factors, marital status, nature of work; to clarify the medical, social and labor history.

Slide No. 29

Slide Description:

On physical examination, the physician should identify POM and signs of secondary hypertension. On physical examination, the physician should identify POM and signs of secondary hypertension. It is imperative to measure the patient's height, weight, waist, calculate the BMI. The secondary nature of hypertension may be indicated by the following data revealed during the examination: Symptoms of the disease or Itsenko-Cushing's syndrome; Neurofibromatosis of the skin (with pheochromocytoma); Kidney enlargement (polycystic, masses); Weakened or delayed pulse in the femoral artery and decreased 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 - murmurs over the abdominal aorta, renal arteries (renal artery stenosis - vasorenal hypertension).

Slide No. 30

Slide Description:

POM should be suspected in: POM should be suspected in: brain - auscultation of murmurs above the carotid arteries, motor and sensory disorders; retina of the eye - changes in the vessels of the fundus; heart - increased apical impulse, rhythm disturbances, the presence of CHF symptoms (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.

Slide No. 31

Slide Description:

Fasting Plasma Glycemia Fasting Plasma Glycemia Test for Glucose Tolerance Total CL LDL CL HDL CL TG Potassium Uric acid Creatinine Estimated creatinine clearance or glomerular filtration rate Hemoglobin and hematocrit Urine analysis (with determination of microalbuminuria); quantitative analysis of proteinuria.

Slide No. 32

Slide Description:

Slide No. 33

Slide Description:

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 corresponding 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 corresponding organs, kidney biopsy.

Slide No. 34

Slide Description:

Slide No. 35

Slide Description:

Antihypertensive therapy should be ongoing; Antihypertensive therapy should be ongoing; 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.

Slide No. 36

Slide Description:

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 2 receptor blockers and beta-blockers. Drugs of these classes can be used both as monotherapy and low-dose fixed combinations.

Slide No. 37

Slide Description:

Slide No. 38

Slide Description:

Slide No. 39

Slide Description:

Slide No. 40

Slide Description:

Slide No. 41

Slide Description:

Slide No. 42

Slide Description:

Regardless of the choice of drugs, the use of monotherapy can only achieve the desired level in a limited number of patients. Most patients need more than one antihypertensive drug to reach their target BP. Initial therapy can be carried out with the help of both monotherapy and the combined use of two drugs in 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 CVD complications. Preference should be given to the combined use of two drugs in low doses in cases where the initial 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 only achieve the desired level in a limited number of patients. Most patients need more than one antihypertensive drug to reach their target BP. Initial therapy can be carried out with the help of both monotherapy and the combined use of two drugs in 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 CVD complications. Preference should be given to the combined use of two drugs in low doses in cases where the initial blood pressure corresponds to 2 or 3 degrees of hypertension or the overall risk of complications is high.

Slide No. 43

Slide Description:

A fixed-dose combination of drugs is preferred because simplifying treatment has a better chance of adhering to therapy. A fixed-dose combination of drugs is preferred because simplifying treatment has a better chance of adhering to therapy. A decrease 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.

Slide No. 44

Slide Description:

Whenever possible, patients with type 2 diabetes should use an intensive regimen of non-drug interventions, with particular attention to weight loss and restriction of sodium chloride intake. Whenever possible, patients with type 2 diabetes should use an intensive regimen of non-drug interventions, with particular attention to weight loss and restriction of sodium chloride intake. The target blood pressure is 130/80 mm Hg. Antihypertensive therapy is prescribed already with hypertension 1 tbsp. Diuretics and beta-blockers should not be used in the first stage of treatment. they aggravate insulin resistance and necessitate an increase in doses or the number of antihyperglycemic drugs.

Slide No. 45

Slide Description:

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 should take into account the need for interventions that address all risk factors, including the appointment of statins.

Slide No. 46

Slide Description:

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

Slide Description:

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

Slide No. 49

Slide Description:

In patients with atrial fibrillation, strict monitoring of antihypertensive therapy with anticoagulant therapy is required. In patients with atrial fibrillation, strict monitoring of antihypertensive therapy with anticoagulant therapy is required. Administration of angiotensin 2 receptor blockers is considered preferable in patients with paroxysms of atrial fibrillation. With a constant form of atrial fibrillation, beta-blockers and nondihydropyridine calcium channel blockers (verapamil, diltiazem), which reduce the ventricular rate, retain their importance.

Slide No. 50

Slide Description:

Indications for planned hospitalization: Indications for planned hospitalization: - The need for special, more 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 hypertension. Indications for emergency hospitalization: GC that does not stop at the prehospital stage; GC with severe manifestations of hypertensive encephalopathy; Complications of hypertension requiring intensive therapy and constant medical supervision: cerebral stroke, subarachnoid hemorrhage, acute visual impairment, pulmonary edema, etc.

Slide No. 51

Slide Description:

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 dysfunctions 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 dysfunctions of the autonomic nervous system.

Slide No. 52

Slide Description:

Neuropsychic stressful situations Neuropsychic stressful situations Intense physical activity Prolonged strenuous work without rest, associated with great responsibility, intake of large amounts of water and salty food on the eve. visual analyzers Alcohol abuse Drinking large amounts of coffee Intense smoking Sudden withdrawal of beta-blockers Abrupt cessation of treatment with clonidine Excessive mental stress, accompanied by lack of sleep Treatment of GCS, NSAIDs, tricyclic antidepressants, sympathomimetic amines

Slide No. 53

Slide Description:

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

Slide No. 54

Slide Description:

HA are divided into 2 large groups: complicated (life-threatening) and not complicated (non-life-threatening). HA are divided into 2 large groups: complicated (life-threatening) and not complicated (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:

Slide No. 55

Slide Description:

Rapidly progressing or malignant hypertension with edema of the optic papilla Rapidly progressing or malignant hypertension with edema of the optic nipple cerebrovascular disease: acute hypertensive encephalopathy ischemic stroke with severe hypertension hemorrhagic stroke acute myocardial infarction or myocardial infarction; unstable angina after coronary artery bypass grafting kidney disease: acute glomerulonephritis renal crisis in systemic connective tissue diseases severe hypertension after kidney transplantation

Slide No. 56

Slide Description:

Excess circulating catecholamines Excess circulating catecholamines crisis pheochromocytomal interaction of food or medications with MAO inhibitors use of sympathomimetic amines "rebound" hypertension after sudden cessation of antihypertensive drugs Eclampsia Surgical diseases: severe hypertension in patients requiring immediate postoperative hemorrhage surgery vascular ligation severe, extensive body burns severe nosebleeds head injuries

Slide Description:

1. Stopping an increase in blood pressure: determine the degree of urgency of starting treatment, choose the drug and the route of its administration, establish the required rate of blood pressure decrease, determine the level of permissible decrease in blood pressure. 1. Stopping an increase in blood pressure: determine the degree of urgency of starting treatment, choose the drug and the route of its administration, establish the required rate of blood pressure decrease, determine the level of permissible decrease in blood pressure. 2. Ensuring adequate control over the patient's condition during the period of lowering blood pressure: timely diagnosis of complications or excessive decrease in blood pressure is required. 3. Consolidation of the achieved effect: prescribe the same drug, with the help of which blood pressure was reduced, if impossible - other antihypertensive drugs, taking into account the mechanism and duration of the selected drugs. 4. Treatment of complications and concomitant diseases.

Slide Description:

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

Slide No. 62

Slide Description:

The most rapid decrease in blood pressure is necessary for dissecting aortic aneurysm (by 25% of the initial in 10-15 minutes, the optimal time to reach the target SBP 100-110 mm Hg - 20 minutes), as well as in acute left ventricular failure. The most rapid decrease in blood pressure is necessary for dissecting aortic aneurysm (by 25% of the initial in 10-15 minutes, the optimal time to reach the target SBP 100-110 mm Hg - 20 minutes), as well as in 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 lower blood pressure and its optimal value is decided together with a neurologist individually for each patient.

Slide No. 63

Slide Description:

Slide No. 64

Slide Description:

1 slide

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 higher, 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).

2 slide

Heredity. 60 genes involved in the development of hypertension have been identified; polymorphism of the gene for angiotensin-II-converting enzyme, angiotensinogen, renin, glucocorticoid receptors is especially important. Overweight The relationship between hypertension, hyperinsulinemia and lipid metabolism disorders (decreased high density lipoproteins, increased low and very low density lipoproteins) and obesity - "metabolic syndrome" has been shown. Diabetes mellitus In diabetes mellitus (especially type II), hypertension occurs 2 times more often than in people without it. Age Consumption of sodium chloride 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 AG

3 slide

Renin-angiotensin system of the myocardium and coronary vessels Tissue AII VESSELS MACROPHAGES FIBROBLAST MYOCYTES NERVOUS END ACE Khimase Norepinephrine AI AII ACE AT1R AT2R AT1R AT2R AT1R Cardiac arthrosis Chromatosis 88: 1 L

4 slide

5 slide

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 Decrease of the baroreceptor mechanism Activation of the vagus nerve center Depressurization and regulation of the fibrosis regulation renin and prostaglandin systems Vascular permeability Circulatory bed Short-term effects Compensatory-adaptive reactions Tissue level Long-term effects Structural rearrangement of target organs

6 slide

Radiographically in hypertension, signs of left ventricular hypertrophy, its hypertrophy with dilatation, atherosclerotic lesions of the aorta, signs of venous congestion in the lungs are determined (Fig. A, b, c).

7 slide

Severe left ventricular hypertrophy. 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. Displacement of the transition zone to the right to V3. Displacement of the electrical axis of the heart to the left, with RI> 12 mm. Oblique displacement segment S-T and inversion of the T wave in I, aVL, V5, V6.

8 slide

Classification of arterial hypertension by the level of arterial pressure (WHO, MTF, 1999) BP, mm Hg. Art. systolic diastolic Optimal pressure

9 slide

Stages of arterial hypertension depending on the target organ damage (WHO, 1996) I st. There are no manifestations 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 changes in blood vessels (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 - aortic dissecting 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.

10 slide

Mechanisms of the hypotensive action of β-blockers Level Nature of action of the central nervous system They block β-adrenergic receptors, enhance the effect of NA on α-adrenergic receptors of the medulla oblongata with inhibition of the activity of the sympathetic NS. β-adrenergic receptors 1. High sensitivity to β-adrenergic receptors, competitive antagonism. 2. Membrane stabilizing activity. 3. Selectivity - selective action on β1-receptors of the heart (cardioselectivity). Nonselective β-blockers act on β1-receptors of the heart and β2-receptors of blood vessels, kidneys, bronchi, smooth muscles. Hemodynamics Negative chronotropic, inotropic effects, decrease in cardiac output, myocardial oxygen consumption, coronary blood flow. The initial increase in OSPS, with long-term therapy, there is an adaptation of the vessels and the normalization of peripheral resistance. Neuro-moral systems Decrease the activity of renin. They increase the release of insulin, decrease the secretion of glucagon.

11 slide

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 Noncardioselective without intrinsic sympathomimetic activity Propranolol 20 - 160 2 - 3 with intrinsic sympathomimetic activity Oxprenolol 20 - 480 2 - 3 with β-adrenergic blocking properties Carvediol 25 - 100 1 Labetalol 200 - 1200 2

12 slide

Systemic effects of ACE inhibitors Effects Effects Cardio-protective effect regression of LVH and myocardiofibrosis; prevention of left ventricular dilatation; anti-ischemic effect; reduced afterload due to arterial vasodilation; reduced preload due to venous vasodilation; antiarrhythmic effect in myocardial ischemia. Vaso-protective effect: suppression of proliferation of smooth muscle cells of arteries; increased endothelium-dependent vasodilation; potentiation of the vasodilatory 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: improving glucose metabolism by increasing the sensitivity of peripheral tissues to insulin; antiatherogenic effect.

13 slide

Therapeutic doses of ACE inhibitors Drug name Therapeutic dose (mg / day) Frequency of administration Captopril 50-150 2 Enalapril (Renitek) 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

14 slide

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 (Cardil) 60-120 3 - 4 2 Long-acting diltiazem 180-360 1

15 slide

The mechanism of action of AT1 receptor blockers is to eliminate the effects of angiotensin II mediated by AT1 receptors and to enhance the effects of AT2 receptor stimulation. DOSES OF AT1-RECEPTOR BLOCKERS Indications for administration are similar to 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

16 slide

Classification and doses of diuretics Name Daily dose, mg Thiazide diuretics Hydrochlorothiazide (dichlothiazide, hypothiazide) 12.5-50 Thiazide-like diuretics Clopamide 10 - 20 Indapamide (arifon) 1.5 - 2.5 Loop diuretics Furosemide 20 - 480 (urea) 25 - 100 Potassium-sparing diuretics Spironolactone (veroshpiron) 25 - 100 Amiloride 5 - 10

17 slide

Classification and doses of α-adrenergic blockers α1-blocking action is possessed by dihydroergocristin, droperidol, carvedilol, labetalol. Name of the drug Release form, dose Daily dose (mg) Non-selective α-adrenergic blockers Pirroxan tab. 0.015 amp. 1.0 ml of 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 (roots) tab. 2-5 mg Bendazolol (glyophene) 1 tab. 20 mg

18 slide

DEATH QUARTET "OBESITY, HYPERTENSION, IMPAIRMENT OF GLUCOSE TOLERANCE, DYSLIPIDEMIA AND THEIR POSSIBLE RELATIONSHIP TO INSULIN RESISTANCE" (C. Isles, 1997) obesity insulin resistance glucose tolerance hypertension dyslipidemia

19 slide

20 slide

A hypertensive crisis is a sudden significant increase in blood pressure, accompanied by the appearance or intensification of disorders in the target organs and the autonomic nervous system. Criteria for a crisis: - a 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 patient's life, require immediate, within 1 hour, decrease in blood pressure). II. Uncomplicated crises (without acute or progressive damage to target organs, pose a potential threat to the patient's life, require a rapid, over several hours, decrease in blood pressure).

21 slide

Kinds of complications of hypertensive crises: Myocardial infarction Stroke Acute dissecting aortic aneurysm acute left ventricular failure Unstable angina Arrhythmias (paroxysmal tachycardia, atrial tachyarrhythmia, ventricular extrasystoles) Transient ischemic attack Eclampsia The acute hypertensive encephalopathy bleeding Acute renal failure TYPES uncomplicated hypertensive crises - Cerebral uncomplicated crisis - Hypothalamic paroxysm (diencephalic-vegetative crisis). - Cardiac uncomplicated crisis. - Increase in SBP to 240 or DBP to 140 mm Hg. - A significant increase in blood pressure in the early postoperative period.

22 slide

Treatment of complicated hypertensive crises Drug Route of administration Onset of action Duration of action Notes Vasodilators Sodium nitroprusside IV drip, 0.25-10 μg / kg (50-100 mg in 250-500 ml of 5% glucose) Immediate slow 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 Especially 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 per hour, then 30 μg / kg per hour After 10-20 min 2-4 hours For subarachnoid hemorrhages

23 slide

Treatment of complicated hypertensive crises Name of the drug Route of administration Onset of action Duration of action Notes Antiadrenergic agents Propranolol IV drip, 2-5 mg at a rate of 0.1 mg / min After 10-20 minutes 2-4 hours With exfoliating aortic aneurysm and coronary syndrome Esmolol IV drip of 250-500 mcg / kg in 1 min for 1 min, then 50-100 mcg / kg for 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 renal failure Magnesium sulfate IV bolus, 5-20 ml 25% solution Through 30-40 minutes 3-4 hours For convulsions, eclampsia of pregnant women

24 slide

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 AB blockade, bradycardia Captopril 12.5 - 25 mg orally or sublingually After 30 minutes Hypotension in patients with renin-dependent hypertension Dibazol 1% solution 4 - 6 ml IM or i.v. 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 i / m Through 15-30 minutes Dizziness, drowsiness Prazosin 0.5-2 mg orally After 30-60 minutes Orthostatic hypotension, tachycardia Labetolol 200-400 mg orally After 30-60 minutes Orthostatic hypotension, bronchoconstriction Propranolol 20-80 mg orally After 30-60 minutes Tachycardia, bronchoconstriction Metoprolol 25-50 mg orally After 304-60 minutes Tachycardia, bronchoconstriction