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ARTERIAL

HYPERTENSION
Definitions

 Elevated arterial blood pressure is a major


cause of premature vascular disease leading
to cerebrovascular events, ischemic heart
disease and peripheral vascular disease.
 Blood pressure is a characteristic of each
individual, like height and weight, with
marked interindividual variation, and has a
continuous distribution.
Definitions
 Hypertension (HTN) or high blood pressure is a
chronic medical condition in which the systemic
arterial blood pressure is elevated.
 It is classified as either primary (essential) or
secondary.
 About 90–95% of cases are termed "primary
hypertension", which refers to high blood pressure
for which no medical cause can be found.
 The remaining 5–10% of cases (Secondary
hypertension) are caused by other conditions that
affect the kidneys, arteries, heart, or endocrine
system.
Definitions

 Hypertension is very common in the


developed world;
 Is present in 20-30% of the adult population;
 Hypertension rates are much higher in black
Africans (40-45% of adults).
Classification of BP levels
(WHO 1999, Russian recommendations 2003)
Category Systolic BP Diastolic
BP
Optimal BP <120 <80
Normal BP 120-129 80-84
High normal BP 130-139 85-89
Hypertension 1 degree 140-159 90-99
Hypertension 2 degree 160-179 100-109
Hypertension 3 degree 180 110
Isolated systolic hypertension 140 <90
How to determine risk groups?
• Prognosis develops not only from BP levels but
also from presence of risk factors (RF), involving
damaged organs (DO) and associated clinical
conditions (ACC)
• This is very important in management of patients
with hypertension and other diseases (diabetes
mellitus, cardiovascular diseases).
Risk stratification
RF Damaged organs ACC
Men>55 years; Hypertrophy of left Cardiovascular
Women>65 years; ventricular; diseases: ischemic or
Smoking; Proteinuria or hemorrhagic stroke,
Cholesterol>5,0 creatininemia 1.2-2.0 transient ischemic
mmol/l; mg/dl; stroke;
Family anamnesis of Atherosclerosis Heart diseases:
early CVD; plaque; myocardial infarction,
Diabetes mellitus Retina arteries stenocardia, coronary
constriction revascularization, heart
insufficiency;
Kidney diseases:
diabetic nephropathy,
renal failure
Peripheral arteries
damage
Distribution AH according risk degrees
Blood Pressure

Degree 1 Degree 2 Degree 3


Risk factors BPs 140-159 or BPs 160-179 or BPs 180 or
BPd 90-99 BPd 100-109 BPd 110

I. NO RF, DO, ACC LOW RISK MIDDLE RISK HIDH RISK

MIDDLE MIDDLE VERY HIGH


II. 1-2 RF RISK RISK RISK

III. 3 and > RF and/or VERY HIGH


HIGH RISK HIGH RISK
DО and/or DM RISK

VERY HIGH VERY HIGH


IV. ACC, DО, RF RISK VERY HIGH RISK
RISK
Risk levels
(risk of stroke or MI during 10 years):

 Low risk (1) = < 15%.


 Middle risk (2) = 15-20%.
 High risk (3) = 20-30%.
 Very high risk (4) = 30% and >.
Determination hypertension stage
• I stage: absence of changes in target organs
• II stage: one or several changes in target organs
• III stage: one or several associated clinical conditions

Examples of clinical conclusions:


• Arterial hypertension, 3d degree, II stage. Dyslipidemia. Hypertrophy of left
ventricle. High risk.
• Arterial hypertension, 3d degree, III stage. CHD. Exertional angina. Very
high risk.
Definitions: measuring of BP
 The blood pressure (BP) of all adult patients should be
assessed at all appropriate visits for determination of
cardiovascular risk and monitoring of antihypertensive
treatment by health care professionals who have been
specifically trained to measure BP accurately.
 BP must be measured after 5 minutes’ resting in seating
position with appropriate cuff size.
 Standing BP should be measured in diabetic and elderly
subjects to exclude orthostatic hypotension.
 When assessing the cardiovascular risk, the average BP
at separate visits is more accurate than measurements
taken at a single visit.
Causes: genetic factors

 BP tends to run in families and children of


hypertensive parents tend to have higher BP.
 There still remains a large unidentified
genetic component.
Causes: fetal factors

 Low birth weight is associated with


subsequent high BP. This relationship may
be due to fetal adaptation to intrauterine
undernutrition with long-term changes in
blood vessel structure or in the function of
crucial hormone system.
Causes: environmental factors

 Obesity. Fat people have higher BP than thin


people. BP must be measured with big cuff.
 Alcohol intake. There is close relationship
between the consumption of alcohol and BP
level.
 Sodium intake. Populations with higher
sodium intakes have higher average BP than
those with lower sodium intake.
 Stress.
Causes:
 Humoral mechanisms. Autonomic nervous
system, renin-angiotensin, natriuretic peptide
and kallikrein-kinin system play a role in the
physiological regulation of short-term
changes in BP.
 Insulin resistance. There is association
between hyperinsulinemia, glucose tolerance,
reduced levels of HDL cholesterol,
hypertriglyceridemia, central obesity and
hypertension.
Secondary hypertension

 Is where BP elevation is the result of a


specific and potentially treatable cause.
Secondary hypertension: causes
 Renal diseases (80%): diabetic nephropathy,
chronic glomerulonephritis, adult polycystic
disease, chronic tubulointerstitial nephritis,
renovascular disease – due to sodium and
water retention, elevation of plasma renin
levels.
 Endocrine causes: Conn’s syndrome, adrenal
hyperplasia, phaeochromocytoma, Cushing’s
syndrome, acromegaly.
 Congenital: coarctation of the aorta
Secondary hypertension: causes

 Drugs: NSAIDs, oral contraceptives, steroids,


sympathomimetics, vasopressin.
 Pregnancy: when the BP increases to >
160/100 mmHg treatment is warranted for the
protection of the mother. It is the most
common causes of maternal death (10 per
milliom pregnancies).
Signs and symptoms

 Accelerated hypertension is associated with


headache, drowsiness, confusion, vision
disorders, nausea, and vomiting symptoms
which are collectively referred to as
hypertensive encephalopathy.
 Hypertensive encephalopathy is caused by
severe small blood vessel congestion and
brain swelling, which is reversible if blood
pressure is lowered.
Pathophysiology
 Сardiac output is raised early in the disease course,
with total peripheral resistance (TPR) normal; over
time cardiac output drops to normal levels but TPR
is increased because of:
- Inability of the kidneys to excrete sodium, resulting in
natriuretic factors such as Atrial Natriuretic Factor
being secreted to promote salt excretion with the
side effect of raising total peripheral resistance;
- An overactive Renin-angiotensin system leads to
vasoconstriction and retention of sodium and water.
The increase in blood volume leads to
hypertension;
- An overactive sympathetic nervous system, leading
to increased stress responses.
Pathophysiology
Pathophysiology

 Changes in the large arteries: thickening of


the media, an increase in collagen,
secondary deposition of calcium, more
pronounced arterial pressure wave;
 Left ventricular hypertrophy, which results
from increased peripheral vascular resistance
and increased left ventricular load, is a
significant prognostic indicator of future
cardiovascular events.
Pathophysiology
Complications
 Cerebrovascular  Fundus showing
disease hypertensive changes
 Coronary artery
disease
 Renal failure
 Peripheral vascular
disease
 Retinopathy
Target-organ damage and end-stage disease.
Examination

 First stage – obligatory examinations all the


patients with hypertension: estimation of
organ-damage and cardio-vascular risk,
exclusion of secondary hypertension;
 Second stage – exposure additional risk
factors and organ-damage, form of
secondary hypertension.
ROUTINE AND OPTIONAL LABORATORY
TESTS FOR THE INVESTIGATION OF
PATIENTS WITH HYPERTENSION
 urinalysis
 blood chemistry (potassium, sodium, and creatinine)
 fasting blood glucose
 fasting total cholesterol and high density lipoprotein cholesterol,
low density lipoprotein cholesterol and triglycerides
 standard 12-lead electrocardiography
 Assess urinary albumin excretion in patients with diabetes
 An echocardiogram for assessment of left ventricular
hypertrophy is useful in selected cases to help define the future
risk of cardiovascular events
 Examination of fundus
 Ultrasound of abdominal cavity
 Indirect automatic BP
measurements can be
made over a 24-hour
period using a measuring
device worn by the
patient.
 They are used to confirm
‘white-coat’ hypertension,
to monitor the response
of patients to drug
treatment etc.
Therapy:
LIFESTYLE MANAGEMENT
Physical Exercise
 For nonhypertensive individuals (to reduce
the possibility of becoming hypertensive) or
for hypertensive patients (to reduce blood
pressure) prescribe the accumulation of 30
min to 60 min of moderate intensity dynamic
exercise (such as walking, jogging, cycling or
swimming) 4 -7 days per week, in addition to
the routine activities of daily living. Higher
intensities of exercise are no more effective.
Therapy:
LIFESTYLE MANAGEMENT
Weight Reduction
 Height, weight, and waist circumference (WC) should be measured
and body mass index (BMI) calculated for all adults.
 Maintenance of a healthy body weight (BMI 18.5 kg/m² to 24.9 kg/m²
and waist circumference of less than 102 cm for men and less than
88 cm for women; waist circumference less than 90 cm for South
Asian men and less than 80 cm for South Asian women) is
recommended for nonhypertensive individuals to prevent
hypertension and for hypertensive patients to reduce blood
pressure. All overweight hypertensive individuals should be advised
to lose weight.
 Weight loss strategies should use a multidisciplinary approach that
includes dietary education, increased physical activity and
behavioural intervention.
Therapy:
LIFESTYLE MANAGEMENT
Alcohol Consumption
 To reduce blood pressure, alcohol consumption
should be in both normotensive and hypertensive
individuals. Healthy adults should limit alcohol
consumption to 2 drinks or less per day, and
consumption should not exceed 14 standard drinks
per week for men and 9 standard drinks per week
for women (one standard drink is considered 13.6 g
or 17.2 ml of ethanol, or approximately 44 mL of 80
proof (40%) spirits, 355 mL of 5% beer or 148 mL of
12% wine).
Therapy:
LIFESTYLE MANAGEMENT
Dietary Recommendations
 It is recommended that hypertensive patients

and normotensive individuals at increased


risk of developing hypertension consume a
diet that emphasizes fruits, vegetables and
low-fat dairy products, dietary and soluble
fiber, whole grains and protein from plant
sources that is reduced in saturated fat and
cholesterol.
Therapy:
LIFESTYLE MANAGEMENT
Salt Intake
 For prevention of hypertension, in addition to

a well-balanced diet, a dietary sodium intake


of less than 100 mmol (2,300 mg) per day is
recommended.
 In hypertensive patients, dietary sodium

intake should be limited to 65 mmol to 100


mmol (1495 mg to 2300 mg) per day.
Therapy:
LIFESTYLE MANAGEMENT
Stress management
 In hypertensive patients in whom stress may

be contributing to blood pressure elevation,


stress management should be considered as
an intervention. Individualized cognitive
behavioural interventions are more likely to
be effective when relaxation techniques are
used.
The aim of treatment

 Decrease the risk of cardiovascular diseases


and chronic renal failure, rate of mortality;
 Influence on risk factors
 Treatment of concomitant diseases
 Correction of high BP
Pharmacological therapy should be
based on the following:
Pharmacological therapy should be
based on the following:
Advantages and disadvantages of drugs used in
hypertension with respect to associated conditions
Diuretics
 Thiazide diuretics reduces the risk of stroke in
patients with hypertension but they have adverse
metabolic effects – increase serum cholesterol,
impair glucose tolerance, hyperuricaemia and
hypokalaemia (hypotiazide 12,5-25mg, arifon
2,5mg).
 Furosemide is not routinely used in treatment of
hypertension.
 Spironolactone (potassium-sparing diuretic) is used
in the treatment of hypertension and hypokalaemia
assocaited with primary hyperaldosteronism.
Angiotensin-converting enzyme (ACE)
inhibitors
 Block the conversion of angiotensin I to
angiotensin II, which is a potent
vasoconstrictor, also block the degradation of
bradykinin, a potent vasodilator.
 Potential side-effects: profound hypotension
following the first dose, dry cough,
deterioration of renal function in case of
severe bilateral renovascular disease.
 Enalapril (10-20 mg), ramipril (2.5-10mg),
lisinopril (10-20 mg) etc.
Calcium-channel blockers

 Cause arteriolar dilatation, reduce the force


of cardiac contraction
 Useful with concomitant IHD
 Side-effects: short-acting agents, headache,
sweating, swelling of the ankles, palpitations,
flushing.
 Amlodipine (5-10mg), felodipine (5-20mg),
long-acting nifedipine (20-90mg).
Beta-adrenoceptor blockers
 Side-effects: bradycardia, bronchospasm,
cold extremities, fatigue, bad dreams,
hallucinations.
 Are useful in treatment of patients with both
hypertension and angina, in younger people
with intolerance to ACE inhibitors and
angiotensin-II receptor antagonists, women of
child-bearing potential.
 Bisoprolol (10-20mg), metoprolol (100-
200mg), propranolol (160-320mg).
Angiotensin-II receptor antagonists

 Selectively block the receptors for


angiotensin II.
 They share many of actions of ACE
inhibitors, don’t have any effect on
bradykinin, do not cause cough.
 Losartan (50-100mg), candersartan (up to 32
mg), telmisartan (20-80mg).
The other agents

 Alpha-blockers: cause postsynaptic a1-


receptor blockade with resulting
vasodilatation. F.e. doxazosin (1-4mg),
longer-acting agent.
 Centrally acting drugs: clonidine, moxonidine;
reserve therapy.
Рекомендации по выбору лекарственных
препаратов для лечения АГ
Абсолютные Относит.
Класс Абсолютные Относитель-
противо- противо-
препаратов показания ные показания
показания показания

Сердечная
Дислипидемия
недостаточ-ность
Сохраненная
Пожилые
Диуретики больные
Диабет Подагра сексуальная
активность у
Систолич.
мужчин
гипертензия

Астма и Дислипидемия
хронический Спортсмены и
Стенокардия Сердечная обструктивный физически
β-блокаторы Перенесенный недостаточ-ность бронхит активные
ИМ Беременность Блокада пациенты
Тахиаритмии Диабет проводящих Болезни
периферических
путей сердцаа сосудов

а - Атриовентрикулярная блокада 2 или 3 степени


Рекомендации по выбору лекарственных
препаратов для лечения АГ
Абсолютные Относит.
Класс Абсолютные Относитель-
противо- противо-
препаратов показания ные показания
показания показания
Сердечная
недостаточ- Беремен-ность
ность Гиперкали-
Двусторонний
Дисфункция емия
Ингибиторы стеноз
ЛЖ Двусторонний
АПФ почечных
Перенесен- стеноз
артерий
ный ИМ почечных
Диабетич. артерий
нефропатия
Стенокардия
Застойная
Пожилые Поражения Блокада
Антагонисты сердечная
больные периферическ проводящих
кальция недостаточнос
Систолич. их сосудов путей сердцаб
ть
гипертензия
б – AV блокада 2 или 3 степени для верапамила или дилтиазема
Рекомендации по выбору лекарственных
препаратов для лечения АГ
Абсолютные Относит.
Класс Абсолютные Относитель-
противо- противо-
препаратов показания ные показания
показания показания
Нарушение
α-адренерги- Гипертрофия Ортостати-
толерант-
ческие предстатель- ческая
ности к
блокаторы ной железы гипотензия
глюкозе
Беремен-ность
Двусторонний
Кашель при
стеноз
Антагонисты приеме Сердечная
почечных
ангиотензина II ингибиторов недостат.
артерий
АПФ
Гиперкали-
емия
Рекомендации по выбору лекарственных
препаратов для лечения АГ
Абсолютные Относит.
Класс Абсолютные Относитель-
противо- противо-
препаратов показания ные показания
показания показания
Метаболичес-
кий синдром A-V блокада 2-
Агонисты Сахарный
ожирение, 3 степени
имидазоли- диабет
нарушение Тяжелая
новых Микро-
толерант- сердечная
рецепторов альбумин-урия
ности к недостат.
глюкозе
Effective combination of drugs

 Diuretic and ACE or angiotensin-II receptor


antagonist.
 Diuretic and beta-adrenoceptor blocker.
 Calcium-channel blocker (digidropiridine group) and
beta-adrenoceptor blocker.
 Calcium-channel blocker and ACE.
Hypertensive crisis

 is severe hypertension (high blood pressure)


with acute impairment of an organ system
(especially the central nervous system,
cardiovascular system and/or the renal
system) and the possibility of irreversible
organ-damage. In case of a hypertensive
emergency, the blood pressure should be
lowered aggressively over minutes to hours
with an antihypertensive agent.
Clinical presentations of hypertensive
emergencies:
 cerebral infarction (24.5%),
 pulmonary edema (22.5%),
 hypertensive encephalopathy (16.3%),
congestive heart failure (12%).
 intracranial hemorrhage
 aortic dissection
 eclampsia
 acute renal failure or insufficiency
 retinopathy
Symptoms as:
Headache, Visual Changes, Papilledema
Chest Pain (MI), Pain to Back (Dissection)
Abdominal Pain - abdominal aneurysmal dissection
Flank Pain - renal disease
Mental Status Changes - stroke,
leukoencephalopathy
Hyperkinetic crises I type

 Sudden onset, excitation, more vegetative


features (hyperemia, tachicardia, polyuria,
moisture of skin)
 Beta-blockers (anaprolin 20-40 mg or egilok
50mg) sublingually
 Calcium-channel blockers (nifedipine 10 mg)
sublingually
 Relanium 5 mg (1-2ml i/m)
Hypokinetic crises II type

 Against a background of late disease stages


with gradual development and hard current;
cerebral and cardiac symptoms are shown
 Calcium-channel blockers (nifedipine 10 mg)
sublingually
 ACE (capoten 12,5 mg) sublingually
 Clofelin 0,15 mg sublingually
Crisis with disturbances in cerebral
vessels
 Dibasol 1% 6-10 ml i/v
 Euphillin 2,4%-10ml i/v
 MgSO4 25%-10ml i/v slowly (vasodilating,
sedative, anticonvulsant mechanism)
Crisis complicated with pulmonary
edema
 Nitroglycerine 20 mg (1%-2ml) i/v tiny very
slowly 8 drops in min: Initial dose 5 µg/min
(Max dose 100 µg/min)
 Nitroprusside 30 mg i/v tiny: Initial dose 0.3
µg/kg/min (Max dose 10µg/kg/min)
 Promedol 2%-1ml i/v
 Lasix 80-120 mg i/v
 Capoten 25-50mg

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