Transcript hypertension

Arterial hypertensions.
Hypertonic disease. Hypertonic
crisis. Ethiology. Clinical
pattern. Daignostics. Principles
of treatment
N. Bilkevych
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Arterial hypertension is defined as rising of
arterial blood pressure excess of 140 mm
Hg systolic one (SBP), and/or excess of 90
mm Hg diastolic blood pressure (DBP).
Recommendations from the Joint National
Committee on the Prevention, Detection,
Evaluation and treatment of High Blood
Pressure (JNC-VI report) now regard a BP
of 140/90 mm Hg as high normal and
130/85 mm Hg as normal.
Epidemiology
Поширеність основних серцевосудинних захворювань в Україні
16%
28%
15%
41%
ЦВЗ - цереброваскулярні захворювання
ІХС - ішемічна хвороба серця
ГХ - гіпертонічна хвороба
Hypertension is one among the most widespread among all cardiovascular diseases.
 15 – 25 % of people in the population have
hypertension + 15 % have bordeline
hypertension.
 Primary hypertension occupies 80 – 95 %
of all arterial hypertensions and 10 % of
them are secondary hypertensions.
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Essential, primary, or idiopathic
hypertension is defined as high BP in
which secondary causes forms are not
present
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Aetiology and pathogenesis:
Overstrain of the central nervous system
nervous-functional disorder in regulation of the
vascular tone
vegetative-endocrine disorders and changes in
the renal regulation of the vascular tone
vasopressor adrenal reaction by which arterioles
of internal organs are narrowed
production of rennin, stimulation of renninangiotensin system and systemic vasodilatation
activation of aldosterone secretion.
Pathogenesis
of AH
Risk-factors
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Non-modified
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Age
Genetics and family history
Sex( male or female)
Family and personal history of hyperlipidaemia
Family and personal history of diabetes
Race
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Modified
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Cigarette smoking, alkohol
Environment (stress, sedentary lifestyle)
Weight (obesity and metabolic syndrome)
Dietary habits (high alcohol intake, high sodium intake, low
potassium intake)
Hypodinamia
Personality
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An assessment of dietary and lifestyle
factors is important. Excessive alcohol use
(more than three or four drinks per day)
and a high sodium intake (typically
defined by a urinary sodium excretion of
more than 150 mmol per day) may
contribute to resistant hypertension; the
frequency of salt sensitivity is increased
among patients who are at least 60 years
of age, patients who are black or obese,
and patients with renal impairment.
Classification
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According to blood
pressure:
- normal: SBP < 130
and DBP < 90 mm of
Hg.
Bordeline
hypertension: SBP =
140-160 and DBP =
90-95 mm of Hg;
- Arterial
hypertension: SBP >
160 and DBP > 95
mm of Hg.
SBP
DBP
Optimal
<120
<80
Normal
<130
<85
High
normal
130-139
85-89
Hyperten
sion
I (mild)
140-159
90-99
II(moderat
e)
160-179
100-109
III (severe) >180
>110
Isolated
systolic
<90
>140
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WHPO classification of arterial hypertension
(1993)
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Stage I – no evident signs of target organ damage
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Stage II – presence of at least one of the following
signs of target organ damage:
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Heart: LVH (diagnosed radiologically, on ECG or by Echocardiography)
Retina: generalized or focal narrowing of retinal arteries
Kidney: microalbuminurua, proteinuria, creatinine<2mg/dl (176 µmol/l)
Vessels: increased IMT or plaques in carotid, iliac, or femoral arteries
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Stage III – signs of severe target organ damage:
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Heart: angina pectoris, myocardial infarction, heart failure
Brain: stroke, TIA, vascular dementia
Retina: haemorrhages, exudates, papilloedema
Kidney: renal insufficiency (creatinine>2mg/ml)
Vessels: dissecting aortic aneurysm, symptomatic occlusive peripheral arterial
disease
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Past medical history
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Duration and previous level of high BP
Indications of secondary hypertension
Family history of renal disease (polycystic kidney)
Renal disease, UTI, haematuria, analgesic abuse (parenchymal renal
disease)
Drug/substance intake: oral contraceptives, liquorice, nasal drops,
cocaine, steroids, NSAID’s, erythropoietin, cyclosporin
Episodes of sweating, headache, anxiety, palpitation
(phaeochromocytoma)
Episodes of muscle weakness (aldosteronism)
Risk factors
Symptoms of organ damage
Previous antihypertensive therapy (drugs used, efficacy, adverse effects)
Personal, family, environmental factors
Clinical manifestation
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Manifestation of
hypertension depends
on:
Course of the disease
Its stage;
Presence of
complications and
crises;
Pathogenetic variant
(benign and maligant).
The main objective sign
of the disease is elevated
arterial pressure (over
140/90 mm Hg) . Blood
pressure is liable in early
stage of the disease but
later stabilizes.
I stage
Complaints:
 may be abcent
 patients would usually complain of neurotic disorders:
general weakness, impaired work capacity, inability to
concentrate during work, deranged sleep, trancient
headache, e feeling of heaviness in the heart, vertigo,
noise in the ears, and sometimes palpitation, hain in
heart region. Exertional dyspnoea develops later.
Data of objective examination
 Signs if lesions of internal organs are abcent
 Stable or trancient elevation of BP
II stage
Complaints
 headache
 Dizziness
 Pain in heart region
 Exertional dyspnoea
 Presence of hpertonic crises
 Data of obyective examination : rddness of skin, sweating, decreased tolerance
to physical load.
 Palpation: Ps – firm and tense, fast. Apex beat is expanded and displaced leftward
and downward.
 Percussion: widened vascular bundle, displacement of the left border of relative
cardiac dullness.
 Auscultation: The second heart sound is accentuated over the aorta. Systolic
murmur over heart apex
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There are signs of internal ograns without functional disorders:
Hypertrophty of the left ventricle (according to data of ECG and X-ray, ultrasound
examination).
Generalized or focal narrowing of retinal vessels.
Microalbumiuria, proteinuria and/ormild elevation of blood plasma creatinin (up to
177 mkm/l).
III stage
High, stable elevation of BP
 Development of complications:
- Myocardial infarction
- Heart failure
- Insult
- Trancient ischemic attack
- Retinal hemorrhage
- Dissecting aortic aneurism
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The set if obvious examinations:
Complete blood count;
 Urinalyses;
- Biochemical blood serum tests;
- Urine analyses ny Nechyporenco
Zymnitsky;
- ECG, ultrasound of a heart;
- ultrasound of kidneys;
- chest X-ray;
- Ophthalmoskopy.
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and
Complete blood count and
biochemical lab tests:
- In I stage there are no changes;
- During crisis – trancient leucocitosis,
dys- and hyperlipidemia, elevated
level of K+, creatinin and urea
 In III stage – stable changes,
azotaemia.
 Examination
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In
III
nicturia
of urine:
stage
isohyposthenuria,
ECG
І st. – specific signs are abcent.
 ІІ – ІІІ st . – hypertrophy of the left
ventricle, heart electrical axis is
deviated leftward,
Rv5-6>Rv4, elevation of ST, biphasic Т
(+-)
Increased amplitude of R in left leads
and S - in right leads.
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ECG in hypertrophy of the left ventricle
Ultrasoung examination of hypertensive heart (B- and Mmodes)
Left-ventricular hypretrophy on X-ray
Symptoms of organs damage
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Heart: palpitations, chest pain, shortness of breath, swollen ankles
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Brain and eyes: headaches, vertigo, impaired vision, TIA’s, sensory or motor deficit
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Kidney: thirst, polyuria, nocturia, haematuria
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Peripheral arteries: cold extremities, intermittent claudication
Brain: murmurs over neck arteries, motor or sensory deficits
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Eyes: funduscopic abnormalities
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Heart: location and characteristics of apical impulse, abnormal cardiac rhythms,
ventricular gallop, pulmonary rales, peripheral oedema
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Peripheral arteries: absence, reduction, or asymmetry of pulses, cold extremities,
ischaemic skin lesions
Damage to internal organs
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The adverse effects of hypertension principally involve the
blood vessels, the central nervous system, the retina, the
heart and the kidneys, and can often be detected by simple
clinical means.
Blood vessels
In larger arteries (over 1 mm in diameter) the internal elastic
lamina is thickened, smooth muscle is hypertrophied and
fibrous tissue is deposited. The vessels dilate and become
tortuous and their walls become less compliant.
Central nervous system
Stroke is a common complication of hypertension and may be
due to cerebral haemorrhage or cerebral infarction.
Hypertensive encephalopathy is a rare condition characterised
by high blood pressure and neurological symptoms, including
transient disturbances of speech or vision, paraesthesiae,
disorientation, fits and loss of consciousness.
Kidneys
Long-standing hypertension may cause proteinuria and
progressive renal failure by damaging the renal vasculature.
HYPERTENSIVE RETINOPATHY
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I degree: Arteriolar
thickening, tortuosity and
increased reflectiveness
('silver wiring') II degree:
plus constriction of veins
at arterial crossings
('arteriovenous nipping')
III degree: plus evidence
of retinal ischaemia
(flame-shaped or blot
haemorrhages and 'cotton
wool' exudates) IV degree:
plus papilloedema
Hypertensive retinopaty
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The excess cardiac mortality and
morbidity associated with
hypertension is largely due to a
higher incidence of coronary
artery disease. High blood
pressure places a pressure load
on the heart and may lead to left
ventricular hypertrophy with a
forceful apex beat and fourth
heart sound.
Atrial fibrillation is common and
may be due to diastolic
dysfunction caused by left
ventricular hypertrophy or the
effects of coronary artery disease.
Severe hypertension can cause
left ventricular failure in the
absence of coronary artery
disease, particularly when renal
function, and therefore sodium
excretion, is impaired.
Heart
Secondary hypertension
CAUSES OF SECONDARY HYPERTENSION
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Alcohol
Pregnancy (pre-eclampsia)
Renal disease
• Renal vascular disease
• Parenchymal renal disease,
particularly glomerulonephritis
• Polycystic kidney disease
Endocrine disease
Phaeochromocytoma
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Cushing's syndrome
Primary hyperaldosteronism
(Conn's syndrome)
Hyperparathyroidism
Acromegaly
Primary hypothyroidism
Thyrotoxicosis
Congenital adrenal hyperplasia
due to 11 -p-hydroxylase or
17-hydroxylase deficiency
Classification of secondary
hypertension
Renoparenchimatous (pyelonephritis,
glomerulonephritis) or renovascular (renal artery
stenosis) disease
 Endocrine disease (Phaeochomocytoma, Cusings
syndrome, Conn’s syndrome, Acromegaly and
hypothyroidism etc.)
 Due to disorders of emodynamics (coarctation of the
aorta, heart valvular diseases, atherosclerosis)
 Neurogenic (brain commotion, tumor etc.)
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Induced by exogenic factors (noise, heat etc.)
Complication of pregnancy
 Iatrogenic:
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hypertensions induces by surgical treatment
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Hormonal / oral contraceptive, corticosteroids etc.
Differential features of symptomatic
hypertension
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Age less than 20 years or more than 60;
quick elevation of BP and its stable high level
very high BP (> 220/120 mm of Hg);
- malignant course of hypertension;
- sympathoadrenal crisesеs;
- renal diseases in anamnesis;
development
of
hypertension
during
pregnancy;
- appearance of changes in patient’s urine.
Features of secondary hypentensions
Renoparenchimatous:
- acute and chronic pyelonephritis, glomerulonephritis
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- nephritis in collagenoses (endarteriiris nodosa, lupus
erytematodus, scleroderma etc);
- Development of AH is possible in unilateral lesion
(nephrolothiasis, hydronephris, cancer)
Special appention is paid for anamnesis and data of objective
examination
 Endocrine hypertension
 Develops in 2- 3 % of cases.
 They are combined with:
- Sympathoadrenal crises;
myasthenia;
changes in urine;
- abecity;
- thyrotoxicosis.
Hemodynamic hypertensions
Are combined with dieases of heart and vessels.
Main causes:
- Atherosclerosis of aorta; coarctation of aorta,
aortal incompetence, open aortal duct;
- Complete AV block;
- erhthraemia,
- Bronchial asthma;
- Heart failure
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There AH are easly diagnosed whe the patient is
exemined completely.
Hypertensive crisis
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Essential hypertension is characterized by periodically recurring
trancient elevations of arterial pressure (hypertensive crisis).
Development of such crises is preceded by psychic traumas, nervous
overstrain, variations in atmospheric pressure, etc.
Hypertensive crisis develops with a sudden elevation of the arterial
pressure that can persist from a few hours to several days. The
crisis is manifested by sharp headache, feeling of heat, perspiration,
palpitation, giddiness, piercing pain in the heart, sometimes by
deranged vision, nausea, aid vomiting. In severe crisis, the patient
may lose consciousness. The patient is excited, haunted by fears, or
is indifferent, somnolent, and inhibited. Auscultation of the heart
reveals accentuated second sound over the aorta, and also
tachycardia. The pulse is accelerated but can remain unchanged or
even decelerated; its tension increases. Arterial pressure increases
significantly. ECG shows decreased S-T interval and flattening of the
T wave. In the late stages of the disease, with organic changes in
the vessels, cerebral circulation may be deranged during crisis;
myocardial infarction and acute left-ventricular failure may also
develop.
Complications of hypertonic crisis
Cardial:
- acute or chronic heart failure;
- accelerated development of atherosclerosis of
caoronary arteries followed by symptoms of
angina pectoris and myocardial infarction;
- arrhythmias.
 Aortal:
- atherosclerosis ;
- dissecting aortal aneurism.
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Cerebral:
- atherosclerosis of
cerebral vessels and
impaired cerebral
circulation
(encephalopathy);
- dynamic and organic
disorders of brain
circulation і органічні
Ocular:
- retinal hemorrhage and
its separation;
- decreased vision (edema
of ophthalmic nerve).
Treatment
Modification of life-style
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Diet (Decreased salt intake to
4-6 g/day, alkohol, animal
fats).
Decreased body weight.
Avoiding of smoking.
Dynamical physical
examinations.
Phytotherapy, acopuncture,
psychtherapy, authotrening
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Influence of modification of
life-style of the course of the
disease:
Decreased body weight - 5-20
mm of Hg/10 kg of lost weight
Diet – 8-14 mm of Hg
Decreased salt intake (6 g per
day) – 2-8 mm of Hg
Physical activity (30 min per
day) – 4-9 mm of Hg
Decreased alkohol
consumption (to 1 ounce per
day) – 2-4 mm of Hg
Appropriate lifestyle measures may obviate the
need for drug therapy in patients with
borderline hypertension, reduce the dose and/or
the number of drugs required in patients with
established hypertension, and directly reduce
cardiovascular risk.
 Correcting obesity, reducing alcohol intake,
restricting salt intake, taking regular physical
exercise and increasing consumption of fruit and
vegetables can all lower blood pressure.
Moreover, quitting smoking, eating oily fish and
adopting a diet that is low in saturated fat may
produce further reductions in cardiovascular risk.
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Aims of antihypertensive
medicamentous therapy
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Immediate: achieve target BP levels
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Intermediate: prevent target organs
disfuction (TOD) or regression of TOD
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Final: improve long-term prognosis
Main groups of hypertensive drugs
Diuretics
 -blockers
 Ca- channels antagonists
 Angiotensine-converting enzyme inhibitors
 Blockers of angiotensine-II receptors
 ά1-adrenoblochers
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TARGET <140 mm Hg systolic and < 90 mmHg diastolic
Lifestyle modification
therapy
Thiazide
diuretic
ACE-I
ARB
Long-acting
CCB
Dual Combination
Triple or Quadruple
Therapy
* Not indicated as first line therapy over 60
Betablocker*