Classification of hypertension according to blood pressure level

 

Category	SBP(mmHg)		DBP(mmHg)
Optimal	< 120	and	< 80
Normal BP	120-129	and/or	80-84
High normal	130-139	and/or	85-89
Grade I hypertension	140-159	and/or	90-99
Grade II hypertension	160-179	and/or	100-109
Grade III hypertension	³180	and/or	³110
Grade IV hypertension	³140	and	< 90

Classification of hypertension by extent of organ damage

Stage I	No objective signs of organic changes
Stage II	At least one of the following signs of organ involvement without symptoms or dysfunction: - left ventricular hypertrophy (electrocardiogram, ultrasound); - generalized and focal narrowing of the retinal arteries; - proteinuria and/or slight elevation of plasma creatinine concentration (1,2- 2,0 mg/dl or to 177 mmol/1); - ultrasound or radiological evidence of atherosclerotic plaque (carotid arteries, aorta, iliac and femoral arteries).
Stage III	Both symptoms and signs have appeared as result of organ damage. These include: - heart (myocardial infarction, heart failure); - brain (stroke, transient ischemic attack, encephalopathy, vascular dimension); - optic fundi (retinal hemorrhages and exudates with or without papillodema); - kidney(plasma creatinine concentration more than 2,0 mg/dl or 177 mmol/1); - vessels (dissecting aneurysm, symptomatic arterial occlusive diseases).

 

Clinical features

Complaints: pain at the heart, palpitation, headache, dizziness, disorder of vision. At the expressed left ventricular failure - attacks of dyspnea.

Objective examination. General patient condition is usually satisfactory. On progression of disease and appearance of complication general patient's condition may be from middle grave to grave (hypertension crisis, acute and chronic heart failure and cerebral attacks).

The color of the skin may be hyperemic. As usually the patients are overweight. At development of heart failure acrocyanosis and peripheral edema are observed.

Objective examination of the cardiovascular system. Apex beat is displaced to the left and downwards, diffuse, high. Displacement of the left border of the relative cardiac dullness to the left is observed. Increased loudness of the first heart sound at the heart apex and accentuated second heart sound over aorta are heard. At the presence of heart failure the gallop rhythm is heard. Blood pressure > 140/90 mm Hg. Pulse is firm tension (p. durus).

Protocol of diagnostic procedures for patients with hypertension I-II stages

Obligatory examination:

- inquiry;

- physical examination: measurement of blood pressure on both hands, measurement of blood pressure on lower extremities at persons younger 45 years; measurement of body weight of and waist circumference;

- laboratory routine examination hemoglobin and hematocrit, clinical urine analysis, Nechiporenko's test, Zemnicky's test, biochemical blood analysis: serum creatinine, serum potassium, serum total cholesterol, serum low density lipoprotein (LDL) cholesterol, serum high density lipoprotein (HDL) cholesterol, fasting serum triglycerides;

- ECG in 12 standard leads;

- echocardiography;

- fundoscopic examination.

Special examination:

- determination of microalbuminuria;

- daily proteinuria;

- ambulatory blood pressure measurement using monitor;

- ultrasound examination of kidneys.

Protocol of diagnostic procedures for patients with hypertension III stages

Obligatory examination:

- inquiry;

- physical examination: - measurement of blood pressure on both hands, measurement of blood pressure on lower extremities at persons younger 40 years;

- measurement of body weight and waist circumference;

- laboratory routine examination hemoglobin and hematocrit, clinical urine analysis, Nechiporenko's test, Zemnicky's test, biochemical blood analysis: serum creatinine, serum potassium, serum total cholesterol, serum low density lipoprotein (LDL) cholesterol, serum high density lipoprotein (HDL) cholesterol, fasting serum triglycerides;

- ECG in 12 standard leads;

- echocardiography;

- examination of the eyes;

- X-ray examination of the chest;

- ultrasound examination of kidneys.

Special examination:

- ambulatory blood pressure measurement using monitor;

- doppler-ultrasound scanner of extracranial vessels;

- computer tomography and magnitoresonance tomography of head;

- in case of coronary heart diseases - cardioventnculography.

Additional methods of examination

Clinical blood analysis: at the prolonged course of hypertension occur hypertensive polycytemia - increased hemoglobin and hematocrit are possible.

Biochemical blood analysis: at development of kidney failure there is increasing level of creatinine.

Clinical urine analyses: at development of nephroangiosclerosis and renal failure - proteinuria, microhematuria, hypo-, isostenuria in Zimnitsky's test.

ECG: the left ventricle hypertrophy, depressed ST-segment, inverted or two-phase T-wave in the 1st and 2nd standard, V₅-V₆ chest leads.

X-ray examination of heart. In the initial period of hypertrophy, rounding of apex of the left ventricle is find out. All chambers of heart are dilated in the late stages.

Echocardiography: hypertrophy of the interventricular septum and the back wail of the left ventricle, decrease of contractility of the myocardium, increase end systolic and diastolic dimensions of the left ventricle.

Ophthalmoscopy is revealed angioretinopathy.

 

Literature

1. Internal diseases an introductory course. - Vasilenko V., Grebenev A. - M.: Mir. Publishers, 1990. - 647 p

2. Propedeutics to internal medicine. Part 1.-Vinnytsya: NOVA KNYHA, 2006.- 424 p.

3. Propedeutics to internal medicine. Part 2.-Vinnytsya: NOVA KNYHA, 2007.- 264 p.

4. Introduction to the course of internal diseases. Book 1. Diagnosis: [Textbook/Zh.D. Semidotskaya, O.S. Bilchenko, et al.].-Kharkiv: KSMU, 2005. -312p.

5. Michael Swash Hutchison’s clinical methods / XIX edition. ELBS, 1989. -618p.

6. Mark H., Beers M.D., Robert Berkow The Merck Manual of diagnosis and therapy / XVII edition.- Published by Merk research laboratories, 1999.- 2833 p.

7. Harrison΄s principles off internal medicine / Fauci, Braunwald, Isselbacher and al.-XIV edition. - Vol. 1 and 2. - International edition, 1998.

 

 

Topic 6. Ischemic Heart Diseases, Main Symptoms and Syndromes at Angina pectoris and Myocardial infraction.

Class lasts: 3 hours

Chronological class structure:

Control of initial standard of knowledges- 20 min.

Teacher′s demonstration of practical skills - 60 min.

Sudents′ independent work: - 30 min.

Control of ultimate standard of knowledges- 15 min.

Sum up of the class, homework- 10 min.

Questions for theoretical preparation: Determination of Ischemic Heart Diseases. Main pathogenesis mechanisms of Ischemic Heart Diseases, Basic risk factors of Ischemic Heart Diseases. Modern classification of Ischemic Heart Diseases. Determination and main symptoms of angina pectoris. Functional classes of angina pectoris. Objective diagnostic methods of angina pectoris (ECG, Monitor- controlling 24 hours –ECG, Exercise test, Scintigraphy of heart, Coranarigraphy). Unstable angina pectoris, definition of unstable angina pectoris and main clinical signs and symptoms of unstable angina pectoris. Determination of acute coronary symptoms. Determination of main clinical signs of acute myocardial infraction. Physical examination methods of patients with acute myocardial infraction. Stages of myocardial infraction. ECG-changes in different forms of myocardial infraction. Modern bio-markers of necrosis of myocardium.

ISCHEMIC HEART DISEASE

Ischemic (coronary)heart disease (IHD)- define as acute and chronic heart damage, caused due to diminishing or stopping blood delivery to myocardium. Disease of the coronary arteries is almost always due to atheroma and its complications, particularly thrombosis.

Etiology and pathogenesis

Atherosclerosis of coronary arteries; the degree of its expression is different -from small wall affection to complete occlusion of vessel.

Spasm of coronary arteries develops, as a rule, on a background of atherosclerosis of coronary arteries. The physical overloading, mental stress provokes the development of clinical features of IHD.

The main pathophysiological mechanism of IHD is imbalance between the demand myocardium in oxygen and possibilities of coronary arteries satisfied the myocardium by adequate amount of blood.

The followings mechanisms are involved in pathological process:

- mechanical occlusion of coronary arteries due to an atherosclerotic process;

- dynamic occlusion of coronary arteries due to coronarospasm;

- activation of thrombocytes aggregation with development of microagregates in microcirculation;

- promotion of production the pro-coagulating factors, insufficiently level of prostacyclin and endothelin- derived relaxing factor;

- increasing of demand myocardium in oxygen under influencing of the intensive physical loading, mental stress, resulting in the high level catecholamines in blood caused cardiotoxic action;

- insufficiency of collateral circulation of blood;

- activation of the lipid peroxidation;

- activation of immune mechanisms.

Thus the pathological substrate of IHD is almost atheroma narrowing of the coronary arteries. Atheroma or atherosclerosis is a focal disease of the arterial intima. There are some stages of evolution of atherosclerotic process. Initial stage is fatty streaks, which develop as circulating monocytes migrate into the intima take up oxidized low density lipoprotein from the plasma and become lipid foam cells. As these foams cells die extracellular lipid pools appear. Smooth muscle cells then migrate into and proliferate within the plaque. A mature fibrinolipid plaque has a core extracellular lipid, separated from the lumen by a thick cap of a collagen-rich fibrous tissue. Such plaque may narrow the lumen of the vessel and often precipitate local vasospasm and thrombosis. The luminal diameter of a coronary artery must be decreased by at least 50 % to 70 % before blood flows becomes inadequate to meet the metabolic demands of the heart during exercise or stress.

The evolution of the atheromatous plague corresponds with clinical forms of IHD. The principal cause of stable angina is atherosclerosis involving at least one large epicardial artery that limited coronary flow under some condition. Stable angina is related to a fixed obstruction and it is usually precipitated by an increase in myocardial oxyden demand (demanded ischemia).

Unstable angina is defined as an obstruction of at least one major epicardial artery that occupies at least 70 % of the artery's cross-sectional diameter or an obstruction of the left main coronary artery that occupies at last 50 % of its diameter. Episodes of myocardial ischemia are due to abrupt reduction in coronary blood flow results from plaque rupture, rapid growth of the lesion or incomplete occlusion of the vessel. Unstable angina is a transitory condition. A platelet rich thrombus forms rapidly around the site of the rupture, reducing, but not usually occluding the blood flow in the vessel.

Myocardial infarction is almost always due to the formation of occlusive thrombus at the site of rupture of an atheromatous plaque in a coronary artery. The affected artery is more commonly completely occluded, usually by a fibrin-rich "red" thrombus.

Sudden death in most cases is attributable to IHD and is usually due to arrhitmia or asystole (ventricular fibrillation, sinoatrial block, complete AV-block) related to acute coronary syndrome, heart failure or scarring from a previous myocardial infarction.

Classification of ischemic heart disease (IHD)

1. Sudden cardiac death.

2. Angina pectoris:

stable angina pectoris;

vasospastic angina (Princmetala's);

unstable angina.

3. Myocardial infarction (Ml):

acute Q-wave Ml;

acute non-Q-wave MI;

-subendocardial MI;

acute MI (undetected);

- recurrent MI (3-28 days);

- repeated MI (after 28 days).

4. Postinfarction cardiosclerosis faction.

6. Cardiac arrhythmia.

7. Painless form of the IHD.

STABLE ANGINA

The 2002 American College of Cardiology/American Heart Association (ACC/AHA) guideline update defined chronic stable angina as a clinical syndrome characterized by discomfort in the chest or adjacent areas caused by myocardial ischemia typically aggravated by exertion or emotional stress and relieved by rest or by nitroglycerin. Patients often describe their symptom as discomfort rather than pain.

Clinical features

The main parameters of pain in patients with stable angina are: location, character, intensity, duration, frequency, radiation, associated symptoms and cause of onset, aggravating and relieving factors. The typical location of angina is mid or lower part of sternum. Less typically, discomfort may occur in the epigastric area. The discomfort is usually described as pressure, tightness, heaviness, strangling, constricting, burning, squeezing, suffocating and crushing.

The severity of the discomfort varies greatly. The pain may radiate in arm to the wrist and fingers, lower jaw or teeth, throat, between the shoulder blades. The duration of the discomfort is brief, not more than 10 min in the majority of cases and more commonly even less. Angina equivalents are common and include dyspnea, faintness, and syncope. Chest discomfort may be accompanied by less specific symptoms such as nausea, burping, restlessness, or a sense impending doom. Frequency of the pain may be different.

An important characteristic is the relation to exercise, specific activities, or emotional stress. Symptoms classically triggered by increased levels of exertion, such as walking up an incline or against a breeze, and rapidly disappear within a few minutes, when these causal factors abate. Exacerbations of symptoms after a heavy meal or work are classical features of angina. Buccal or sublingual nitrates rapidly relieve angina.

For patient with stable angina it is useful to classify the symptoms using a grading system which was devised by the Canadian Cardiovascular Society, based on the severity of the angina stressor.