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.



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.

Hypertension rates are much higher in black Africans (40-45% of adults). Is present in 20-30% of the adult population.Definitions    Hypertension is very common in the developed world. .


Classification of BP levels (WHO 1999. Russian recommendations 2003) Category Optimal BP Normal BP High normal BP Hypertension 1 degree Hypertension 2 degree Hypertension 3 degree Isolated systolic hypertension Systolic BP <120 120-129 130-139 140-159 160-179 u180 u140 Diastolic BP <80 80-84 85-89 90-99 100-109 u110 <90 .

cardiovascular diseases). involving damaged organs (DO) and associated clinical conditions (ACC) ‡ This is very important in management of patients with hypertension and other diseases (diabetes mellitus. . diseases).How to determine risk groups? ‡ Prognosis develops not only from BP levels but also from presence of risk factors (RF).

Retina arteries constriction ACC Cardiovascular diseases: ischemic or hemorrhagic stroke. Proteinuria or creatininemia 1. renal failure Peripheral arteries damage Retinopathy . coronary revascularization. transient ischemic stroke. Atherosclerosis plaque. Kidney diseases: diabetic nephropathy. Cholesterol>5. stenocardia. Diabetes mellitus Damaged organs Hypertrophy of left ventricular. Family anamnesis of early CVD. heart insufficiency. Smoking.0 mg/dl.2-2.0 mmol/l. Women>65 years.Risk stratification RF Men>55 years. Heart diseases: myocardial infarction.

RF ACC. NO RF. D . DO. 1-2 RF 1III.Distribution AH according risk degrees Blood Pressure Risk factors I. ACC II. Degree 1 BPs 140-159 or 140BPd 90-99 90LOW RISK MIDDLE RISK Degree 2 BPs 160-179 or 160BPd 100-109 100MIDDLE RISK MIDDLE RISK Degree 3 BPs u180 or BPd u110 HIDH RISK VERY HIGH RISK HIGH RISK HIGH RISK VERY HIGH RISK VERY HIGH RISK VERY HIGH RISK VERY HIGH RISK . ACC. 3 and > RF and/or and/ D and/or DM and/ IV.

Risk levels (risk of stroke or MI during 10 years): years):  Low risk (1) = < 15%. 20 Very high risk (4) = 30% and >.  Middle risk (2) = 15-20%. >. . 15 High risk (3) = 20-30%.

. Hypertrophy of left stage.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. ‡ Arterial hypertension. Very III stage. 3d degree. High risk. II stage. III stage. CHD. high risk. 3d degree. Dyslipidemia. . Exertional angina. ventricle.

the average BP at separate visits is more accurate than measurements taken at a single visit. When assessing the cardiovascular risk. BP must be measured after 5 minutes¶ resting in seating position with appropriate cuff size.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. . Standing BP should be measured in diabetic and elderly subjects to exclude orthostatic hypotension.

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. .

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: fetal factors  Low birth weight is associated with subsequent high BP.

Populations with higher sodium intakes have higher average BP than those with lower sodium intake. Fat people have higher BP than thin people. Sodium intake. Alcohol intake. Stress. . There is close relationship between the consumption of alcohol and BP level. BP must be measured with big cuff.Causes: environmental factors     Obesity.

There is association between hyperinsulinemia. glucose tolerance. Autonomic nervous system. . central obesity and hypertension. natriuretic peptide and kallikrein-kinin system play a role in the physiological regulation of short-term changes in BP. hypertriglyceridemia. Insulin resistance.Causes:   Humoral mechanisms. renin-angiotensin. reduced levels of HDL cholesterol.

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).

vision disorders. which is reversible if blood pressure is lowered. confusion.Signs and symptoms   Accelerated hypertension is associated with headache. Hypertensive encephalopathy is caused by severe small blood vessel congestion and brain swelling. nausea. and vomiting symptoms which are collectively referred to as hypertensive encephalopathy. . drowsiness.

Inability of the kidneys to excrete sodium. .An overactive Renin-angiotensin system leads to vasoconstriction and retention of sodium and water. . The increase in blood volume leads to hypertension. over time cardiac output drops to normal levels but TPR is increased because of: . resulting in natriuretic factors such as Atrial Natriuretic Factor being secreted to promote salt excretion with the side effect of raising total peripheral resistance. leading to increased stress responses. . with total peripheral resistance (TPR) normal.An overactive sympathetic nervous system.Pathophysiology  ardiac output is raised early in the disease course.

Pathophysiology .

Pathophysiology   Changes in the large arteries: thickening of the media. an increase in collagen. more pronounced arterial pressure wave. is a significant prognostic indicator of future cardiovascular events. which results from increased peripheral vascular resistance and increased left ventricular load. secondary deposition of calcium. . Left ventricular hypertrophy.

Pathophysiology .

Complications      Cerebrovascular disease Coronary artery disease Renal failure Peripheral vascular disease Retinopathy  Fundus showing hypertensive changes .


.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. and creatinine) fasting blood glucose fasting total cholesterol and high density lipoprotein cholesterol. sodium. 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 µwhite-coat¶ hypertension. to monitor the response of patients to drug treatment etc.

cycling or swimming) 4 -7 days per week.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. Higher intensities of exercise are no more effective. . in addition to the routine activities of daily living. jogging.

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. . increased physical activity and behavioural intervention. weight.5 kg/m² to 24.Therapy: LIFESTYLE MANAGEMENT Weight Reduction  Height.  Maintenance of a healthy body weight (BMI 18.  Weight loss strategies should use a multidisciplinary approach that includes dietary education. All overweight hypertensive individuals should be advised to lose weight. and waist circumference (WC) should be measured and body mass index (BMI) calculated for all adults.

. or approximately 44 mL of 80 proof (40%) spirits. 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. Healthy adults should limit alcohol consumption to 2 drinks or less per day. alcohol consumption should be in both normotensive and hypertensive individuals.2 ml of ethanol.Therapy: LIFESTYLE MANAGEMENT Alcohol Consumption  To reduce blood pressure. 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. whole grains and protein from plant sources that is reduced in saturated fat and cholesterol. . vegetables and low-fat dairy products. dietary and soluble fiber.

300 mg) per day is recommended. in addition to a well-balanced diet. dietary sodium intake should be limited to 65 mmol to 100 mmol (1495 mg to 2300 mg) per day. a dietary sodium intake of less than 100 mmol (2. .  In hypertensive patients.Therapy: LIFESTYLE MANAGEMENT Salt Intake  For prevention of hypertension.

stress management should be considered as an intervention. Individualized cognitive behavioural interventions are more likely to be effective when relaxation techniques are used. .Therapy: LIFESTYLE MANAGEMENT Stress management  In hypertensive patients in whom stress may be contributing to blood pressure elevation.

The aim of treatment     Decrease the risk of cardiovascular diseases and chronic renal failure. Influence on risk factors Treatment of concomitant diseases Correction of high BP . rate of mortality.

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.5mg). Furosemide is not routinely used in treatment of hypertension. arifon 2. impair glucose tolerance.5-25mg. hyperuricaemia and hypokalaemia (hypotiazide 12. Spironolactone (potassium-sparing diuretic) is used in the treatment of hypertension and hypokalaemia assocaited with primary hyperaldosteronism.

lisinopril (10-20 mg) etc. dry cough. a potent vasodilator.5-10mg). Potential side-effects: profound hypotension following the first dose. also block the degradation of bradykinin.Angiotensin-converting enzyme (ACE) inhibitors    Block the conversion of angiotensin I to angiotensin II. deterioration of renal function in case of severe bilateral renovascular disease. Enalapril (10-20 mg). . which is a potent vasoconstrictor. ramipril (2.

long-acting nifedipine (20-90mg). headache. felodipine (5-20mg). flushing.Calcium-channel blockers     Cause arteriolar dilatation. reduce the force of cardiac contraction Useful with concomitant IHD Side-effects: short-acting agents. Amlodipine (5-10mg). . swelling of the ankles. sweating. palpitations.

Are useful in treatment of patients with both hypertension and angina. Bisoprolol (10-20mg). women of child-bearing potential. fatigue. cold extremities. in younger people with intolerance to ACE inhibitors and angiotensin-II receptor antagonists. hallucinations.Beta-adrenoceptor blockers    Side-effects: bradycardia. metoprolol (100200mg). bad dreams. bronchospasm. . propranolol (160-320mg).

They share many of actions of ACE inhibitors. candersartan (up to 32 mg). . do not cause cough. don¶t have any effect on bradykinin.Angiotensin-II receptor antagonists    Selectively block the receptors for angiotensin II. telmisartan (20-80mg). Losartan (50-100mg).

The other agents   Alpha-blockers: cause postsynaptic a1receptor blockade with resulting vasodilatation. .e. moxonidine. F. longer-acting agent. doxazosin (1-4mg). Centrally acting drugs: clonidine. reserve therapy.

- - . - - . - - - 2 3 .

- - . . ± AV 2 3 . - - - .

- - . - . - - - - II .

. - . - A-V 3 2- .- - .

Effective combination of drugs     Diuretic and ACE or angiotensin-II receptor antagonist. Diuretic and beta-adrenoceptor blocker. . Calcium-channel blocker and ACE. Calcium-channel blocker (digidropiridine group) and beta-adrenoceptor blocker.

cardiovascular system and/or the renal system) and the possibility of irreversible organ-damage. In case of a hypertensive emergency.Hypertensive crisis  is severe hypertension (high blood pressure) with acute impairment of an organ system (especially the central nervous system. the blood pressure should be lowered aggressively over minutes to hours with an antihypertensive agent. .

pulmonary edema (22. intracranial hemorrhage aortic dissection eclampsia acute renal failure or insufficiency retinopathy .3%).Clinical presentations of hypertensive emergencies:         cerebral infarction (24.5%).5%). hypertensive encephalopathy (16. congestive heart failure (12%).

Symptoms as: Headache.renal disease Mental Status Changes . leukoencephalopathy .abdominal aneurysmal dissection Flank Pain . Pain to Back (Dissection) Abdominal Pain . Papilledema Chest Pain (MI).stroke. Visual Changes.

more vegetative features (hyperemia. 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) . tachicardia. excitation.Hyperkinetic crises I type     Sudden onset. polyuria.

cerebral and cardiac symptoms are shown Calcium-channel blockers (nifedipine 10 mg) sublingually ACE (capoten 12.5 mg) sublingually Clofelin 0.Hypokinetic crises II type     Against a background of late disease stages with gradual development and hard current.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. anticonvulsant mechanism) . sedative.

3 g/kg/min (Max dose 10 g/kg/min) Promedol 2%-1ml i/v Lasix 80-120 mg i/v Capoten 25-50mg .Crisis complicated with pulmonary edema      Nitroglycerine 20 mg (1%-2ml) i/v tiny very slowly 8 drops in min: Initial dose 5 g/min (Max dose 100 g/min) Nitroprusside 30 mg i/v tiny: Initial dose 0.

Sign up to vote on this title
UsefulNot useful