Internal Diseases Propedeutics. Part II. Diagnostics of Cardiovascular

Home , Apex beat

Federal budgetary educational establishment of higher education

Ulyanovsk State University

The Institute of medicine, ecology and physical culture

Smirnova A.Yu., Gnoevykh V.V.

INTERNAL DISEASES PROPEDEUTICS

PART II

DIAGNOSTICS OF CARDIOVASCULAR DISEASES

Textbook of Medicine for medicine faculty students

Ulyanovsk, 2016

УДК 811.11(075.8)

БКК 81.432.1-9я73

С50

Reviewers:

Savonenkova L.N. – MD, professor of Department of faculty therapy

Smirnova A.Yu., Gnoevykh V.V. Internal diseases propedeutics (Part II). Diagnostics of cardiovascular diseases: Textbook of Medicine for medicine faculty students/Ulyanovsk: Ulyanovsk State University, 2017.-96

This publication is the second part of “ Internal diseases propedeutics”, which main goal is the practical assistance for students in the development of the fundamentals of clinical diagnosis of diseases of the cardiovascular system. It contains a description of the main methods of laboratory and instrumental diagnostic tests of diseases of the cardiovascular system. The publication is illustrated with charts, drawings and tables . The textbook is intended for students of medical universities.

Smirnova A.Yu., Gnoevykh V.V., 2017

Ulyanovsk State University, 2017

THE CONTENTS OF A TEXT BOOK

QUESTIONING OF PATIENTS WITH WITH CARDIOVASCULAR 5 DISEASES . Main complains of patients with with cardiovascular diseases . 5

EXAMINATION OF PATIENTS WITH WITH CARDIOVASCULAR 9 DISEASES . General inspection 9

Heart palpation 10

Palpation of vessels 14

Heart percussion 15 Defining of relative cardiac dullness borders. 15

Measurement of heart diameter. 18

Defining of vascular bundle borders 18

Defining of heart configuration. 19

Auscultation of the heart and blood vessels. 28

The heart auscultation: heart sounds abnormalities 31

The heart auscultation: heart murmurs 36

Intracardiac murmurs. 36

Extracardiac murmurs 42

Auscultation of vessels 43

Techniques for improving the auscultation 44

Palpation of the radial pulse 45

Blood pressure 48

CIRCULATORY FAILURE 50

HYPERTENSION 62

ATHEROSCLEROSIS. ISCHEMIC HEART DISEASE 75

Angina pectoris 77

Myocardial infarction 78

TEST CONTROL 82

Application 95

References 99

QUESTIONING OF PATIENTS WITH CARDIOVASCULAR DISEASES . Main complains of patients with cardiovascular diseases . Cardinal symptoms of cardiac diseases are chest pain or discomfort, symptoms of heart failure: dyspnea, edema, fatigue, cough and hemoptysis, nocturia; palpitation, syncope. Chest pain is a common presenting symptom of cardiovascular disease and must be characterized carefully. Chest pain may be cardiac (myocardial or pericardial) or noncardiac in etiology. Ischemic pain is usually of sudden onset, located centrally and stabbing or constricting; it may radiate to the left arm, occasionally to the right, into the neck and to the back. It may be brought on by exercise, emotion, fright or sexual intercourse. Angina pectoris usually lasts less than 30 minutes and may be relieved by rest or administration of nitrates. The pain of myocardial infarction usually lasts for more than 30 minutes, often as long as several hours. Site The pain of cardiac ischaemia (angina / acute myocardial infarction) is often felt centrally in the mid-sternal area, sometimes higher up across the chest, and occasionally it may be felt in the epigastric region or at the back between the shoulder blades. The pain over the precordium or the one that a patient can localize with a finger is seldom cardiac. Character Classically, the pain is constricting, squeezing, crushing or pressing and the patient may clench the fist while describing the sensation. It can be numbing, stinging or burning but not sharp, stabbing or shooting. After the initial waxing it remains constant: brief, repetitive pains are not due to cardiac ischaemia. Duration The pain usually lasts for 2-3 minutes but sometimes may linger for 10-15 minutes. It is neither momentary nor lasts for hours. Recurrent episodes with increasing severity (crescendo/unstable angina) last longer than a few minutes, are easily provoked

5 and may result in acute myocardial infarction (cessation of the coronary flow to part of the myocardium leading to ischaemic necrosis). Radiation The pain of angina radiates centrifugally across the chest, up the neck and jaws, and down the arms on both sides through the inner aspect of the left arm and hand is the commonest region. The reason for this radiation of a cardiac pain is that the inferior cervical sympathetic (stellate) ganglion, which receives the cardiac nerve plexus, contributes fibres to the lower brachial plexus. Precipitating and aggravating factors By definition, angina (inadequate coronary flow for the demands of the myocardium at exercise) is provoked by effort of walking briskly, uphill, in the cold or against the wind; by hurrying after meals; by unaccustomed exercise; or by excitement associated with physical and sympathetic activity (sexual intercourse) or caused by anger (verbal interchanges, unpleasant telephone call), fear, frustration and apprehension. Relieving factors Angina is relieved within a couple of minutes by the cessation of the activity that induced it and by nitrates, which dilate small vessels and reduce the afterload (blood pressure) and the preload (venous pressure and cardiac output), and thereby reduce the work of the heart. The pain of oesophageal spasm, which may be confused with angina, may also be relieved by nitrates. The pain that lasts for more than a few minutes after inhalation or sublingual trinitrate is not angina. The pain of unstable angina and myocardial infarction may occur without any provocating factors, is often associated with an increased sympathetic activity (e.g. sweating, tachycardia, pallor, anxiety, etc.), and is not relieved by a nitrate spray. Associated symptoms Breathlessness, sweating, nausea and restlessness may all be due to apprehension and fear but these symptoms can also accompany left heart failure. The pain of acute pericarditis is usually sharper and lasts much longer than that of angina. It is felt over the precordium and referred to the neck. It is little affected by effort

6 but is often aggravated by breathing, turning, twisting, swallowing food, by lying flat in bed, and may lessen if the patient leans forward. In dissecting aneurysm of the aorta, the pain is felt as tearing sensation; its onset is abrupt, and it radiates to the back along the course of the vessel. The signs and symptoms depend on the location and the extent of the dissection. Dyspnea is a subjective sensation of shortness of breath and often is a symptom of cardiac disease, especially in patients with congestive heart failure. Failure of the heart to pump efficiently may lead to the accumulation of blood in the lungs and dyspnoea (an uncomfortable awareness of breathing). Heart failure should be defined in the four categories of the New York Heart Association (Table 1). Table 1. Functional grading of heart disease (New York Heart Association)

Grade I No limitations of activities, i.e. free symptoms Grade II No limitation under resting conditions, but symptoms appear on sever activity Grade III Limitation of activities on mild exertion Grade IV Limitation of activities at rest, restricting the person to bed or chair

As for the chest pain, questions should be asked about its frequency and onset, provocating, aggravating and relieving factors, duration and about the associated symptoms. A suddenly developing dyspnea suggests pulmonary embolism, pneumothorax, acute pulmonary oedema, exposure to toxic fumes, or a haemorrhage in a tumour obstructing a major airway. In heart failure dyspnea reflects pulmonary venous hypertension secondary to a raised left ventricular end-diastolic pressure. Dyspnea occurs classically in a resting patient in the recumbent position and is relieved promptly by sitting upright (orthopnea). With deteriorating left ventricular function, the end-diastolic, left atrial and the pulmonary venous pressures all rise causing interstitial pulmonary

7 oedema and breathlessness. The clinical expression of these events is that the patient is unable to sleep without the use of the increased number of pillows. In the night, such a patient may slip down on the bed and become breathless a few hours after the onset of sleep (paroxysmal nocturnal dyspnea) associated with wheezing, sweating and apprehension. The patient finds relief by sitting on the side of the bed or getting out of the bed and walking a few paces. In chronic pulmonary disease, the patient may also awaken at night but cough and expectoration often precede the dyspnea. Edema. This is helpful in elucidating the etiology of edema. Thus a history of edema of the legs that is most pronounced in the evening is characteristic of heart failure. Fatigue. This is among the most common symptoms in patients with impaired cardiovascular function. Cough and hemoptysis may be associated with cardiac disease, but it may be difficult to differentiate cardiac from pulmonary disease on the basis of these two symptoms alone. A cough, often orthostatic in nature, may be the primary complaint in some patients with pulmonary congestion. Nocturia, secondary to resorption of edema at night, is common in patients with congestive heart failure. Syncope, which may be defined as a loss of consciousness, results most commonly from reduced perfusion of the brain. The most common causes of syncope are in the table 2.

Table 2.

Causes of syncope

Vasodilatation Vasovagal attack, drugs, micturition syncope Cardiac causes Heart block, paroxysmal tachycardia Outflow obstruction Aortic stenosis, hypertrophic obstruction cardiomyopathy (HOCM) Reduced ventricular Pulmonary embolism, atrial myxoma filling

Reduced blood volume Bleeding

EXAMINATION OF PATIENTS WITH WITH CARDIOVASCULAR DISEASES General inspection During general examination attention should be first of all paid to certain objective signs associated with blood congestion in the lesser or the greater circulation circle. In left ventricular heart failure the above described orthopnea position is characteristic. Chronic right ventricular heart failure manifests itself with a number of objective signs caused by venous blood congestion in the greater circulation circle: cyanosis, cavities hydrops (ascites, hydrothorax, hydropericardium), liver enlargement, scrotum and penis edema, etc. " Carotid dance " — pronounced pulsation of the carotid arteries, a symptom Musset — the same rhythmic head swaying to the beat pulsation. Capillary pulse (Quincke's sign) Quincke's sign (pulse) or «capillary pulse» (Quincke Heinrich Irenaeus, 1842-1922, German physician).This sign (actually precapillar pulse) implies rhythmic synchronous with arterial pulse discoloration of the nail bed (expand-ing-narrowing white spot) on lightly pressing on the distal part of the patient's nail by the doctor's nail. Similar phenomenon can also be observed, if you rub the skin on the forehead, thus there is a pulsating spot of hyperemia. Quincke sign is the sign of aortic valve insufficiency. The name «capillary» is not entirely true, because no capillaries but precapillaries pulsate (i.e. arterioles). The reason o f this symptoms is the failure of the aortic valve. Swelling of neck veins is an important sign of venous blood congestion in the greater circulation circle and increase of central venous pressure. The face in patients with right ventricular and total heart failure is puffy, the skin is yellowish-pale with marked cyanosis of the lips, tip of the nose and ears, the mouth is half-opened, eyes are glassy (facies Corvisari). Cardiac edema is localized on the lower extremities, with pressure in the lower leg area is slowly leveling the hole, depends on the force of gravity (in bed mode localized on the sacrum, lower back). If prolonged edema, the skin becomes hard, non-flexible, 9 brownish because of diapedesis of erythrocytes. Cardiac edema decreases in the morning, increases in the evening. Options for edema: anasarca – widespread, extensive peripheral edema, hydrothorax, hydropericardium, ascites. Before palpation and auscultation, the precordium should be inspected. With good lighting, the point of maximal cardiac impulse may be visible. Cardiac impulses are not normally observed in any other area. The normal apical impulse occurs in early systole and is located within an area of approximately 1 cm2 in the fourth to fifth left inter-costal space near the midclavicular line. Inspection of the precordium should reveal any abnormalities of the bony structures (e.g., pectus excavatum) that may displace the heart to produce unusual findings on physical examination. Epigastric pulsation - visible lifting and retraction of the epigastrium, synchronous with the heart activity can be observed in the right ventricular hypertrophy (RVH), pulsations of the abdominal aorta and the liver. Right ventricular pulsation due to RVH is defined under the xiphoid process and becomes more distinct with a deep breath, while the pulsation caused by the abdominal aorta is localized slightly lower and becomes less pronounced with a deep breath. The true liver pulsation, in combination with a positive venous pulse is found in patients with insufficiency of the tricuspid valve. When this defect during systole, there is reverse flow of blood from the right atrium into the inferior caval and hepatic vein, that is why every heartbeat we observe swelling of the liver. Transfer the pulsation of the liver is caused by transmission of heart contractions.

Heart palpation The main goals of heart palpation are: 1. disclosure of ventricular myocardial hypertrophy; 2. disclosure of ventricular dilatation; 3. disclosure of main vessels dilatations (indirectly); 4. disclosure of aortic and left ventricular aneurysms.

The properties of the apex beat (left ventricular) (AB): localization (specify intercostal space and the relation to the left midclavicular line), power (weakened, strengthened), square (limited, diffuse), the amplitude (high-amplitude — lift, low- amplitude), resistance, raise or not. In the norm the apex beat is localized in V intercostal space at 1.5 cm medially from the left midclavicular line, at the position on the left side is shifted by 1-1. 5 cm to the left, staying in the V intercostal space.

Fig. 1. Consequence of heart palpation 1. apex beat; 2. cardiac beat; 3. Epigastric pulsation; 4.aorta; 5.pulmonary atery; 6. the jugular fossa (aorta)

Fig.2 The position of the hands of the doctor at a palpation apex beat. a. tentative palpation; b. the precise localization, square and power The reasons for the displacement AB to the left — left ventricular hypertrophy (LVH), right ventricular hypertrophy (RVH), right-sided pneumothorax and hydrothorax, pleuropericardial adhesions and fibrosis on the left. The reasons for the displacement AB to the right - dextrocardia. The reasons for the displacement AB up — pregnancy, ascites, meteorism, free gas in the abdominal cavity. The reasons for the displacement AB down — visceroptosis, cachexia, post-Natal period. The reasons for the "disappearance" of AB — hydropericardium, left-sided hydrothorax. The reasons for the increase in the area AB (diffuse) - LVH, thin chest, wrinkling the bottom edge of the left lung, enlarged intercostal space and the tumor of the mediastinum. The reasons for the reduction of the AB (limited) — obesity, swelling of subcutaneous tissue, narrow intercostal space, pulmonary emphysema. The reasons for increasing the amplitude and strength of the AB — LVH, physical activity, anxiety, thyrotoxicosis.

Cardiac (right ventricular) pathological epigastric pulsation

Fig. 3. Cardiac (right ventricular) beat and pathological epigastric pulsation. Cardiac (right ventricular) beat (CB) is a normal palpable as a faint pulsation in the IV intercostal space at the left edge of the sternum. When hypertrophy and dilatation of the right ventricle shifts CB in the epigastric region, leading to pathological epigastric pulsation (Fig.3). Thrills in the heart area – is determined by palpation. It is necessary to estimate its localization and relation to the phases of cardiac (systolic or diastolic) cycle. Mitral stenosis, for example, leads to diastolic thrill in the apex of the heart. Aortic stenosis leads to a systolic thrill in the II intercostal space to the left of the sternum . Blood pressure may be measured satisfactorily with a sphygmomanometer of either the aneroid or the mercury type. Examination of the jugular veins and their pulsations allows quite accurate estimation of the central venous pressure, and therefore gives important information about cardiac compensation. Plesh test (Plesh J., 1878-1957, Hungarian therapist), syn.: abdominal- jugular (or hepato-jugular) reflux. Positive Plesh test occurs in patients with CHF. Palm of the hand for short duration (10 seconds) is pressed against the projection area of the liver in the direction from the bottom upwards. Blood is displaced from the liver into the

13 inferior vena cava and then up to the right atrium, which is manifested by swelling of the neck veins and increase of venous pressure. Pressure on the anterior abdominal wall and an increase in venous blood flow to the heart normally, with adequate contractility of the right ventricle is not accompanied by swelling of the neck veins and increase in central venous pressure (CVP). In patients with chronic heart failure, with a decrease in the pumping function of the right ventricle and the congestion in the veins of the systemic circulation, abdominal- jugular test leads to increased swelling of neck veins and increases CVP at least on 4 cm of water column. Positive abdominal-jugular test indirectly reflects not only the deterioration of hemodynamics of the right heart, but also possible increase in left ventricular filling pressure, i.e. severity of bi-ventricular CHF. Evaluation of abdominal-jugular test results in most cases helps to clarify the cause of peripheral edema, especially when patients have no significant neck veins extension or other external signs of right ventricular failure. Positive test results indicate the presence of congestion in the veins of the systemic circulation due to the right ventricular failure. Negative result of the test excludes heart failure as the cause of edema. In these cases, one should think of another genesis of edema (hypooncotic edema, shins deep vein thrombophlebitis, calcium antagonists intake, etc.).

Palpation of vessels Localization of the abdominal aorta pulsation— the lean people, the epigastric region under the xiphoid process, but lower than in prostatic hyperplasia, decreases with a deep breath. Localization of abnormal aortic arch aneurysm pulsation — the jugular fossa or the handle of the sternum, the so — called retrosternal pulsation. Localization of abnormal extension of the ascending part of the aorta pulsation - to the right of the sternum in the second intercostal space.

Fig.4. Consequence of vessel palpation. Examination of arterial pulse. Properties of the pulse at the radial artery (a. radialis). Rate, rhythm, strain, filling, conture, quality of pulse. Equality of pulse on both limbs (Popov-Savelyev's sign). Examples of changes of the pulse: when aortic stenosis is small, slow, rare; with aortic insufficiency – a large, galloping, frequent. In case of arrhythmia, specify its type. Pulse deficiency (pulse deficiency is defined [counted] in the presence of atrial fibrillation, at early premature beats). Arterial pulses can be palpated over the carotid, axillary, brachial, radial, femoral, popliteal, dorsalis pedis, and posterior tibial arteries.

Heart percussion Main goals of heart percussion are: 1. Disclosure of ventricular and auricular dilation; 2. Disclosure of vascular bundle dilation. Defining of relative cardiac dullness borders. At first right, left and upper borders of relative cardiac dullness are defined. It is necessary to obtain beforehand an indirect impression about the level of diaphragm standing which influences the results of percussion defining of relative cardiac dullness size. For this purpose the lower border of the right lung is defined along the midclavicular line which is normally located at the level of rib VI.

The level of diaphragm The right border of relative cardiac dullness

The upper border of relative cardiac The left border of relative cardiac dullness dullness

Fig.5. Starting position and future direction of pleximeter finger percussing the borders of relative cardiac dullness. The right border of relative cardiac dullness , formed by the right atrium (RA), is found by percussing one rib above the found lower lung border (usually in the IV intercostal space), moving vertically placed pleximeter finger strictly along the intercostal space. Normally it situated at the right sternum edge or 1 cm laterally (Fig.5). The left border of relative cardiac dullness formed by the left ventricle (LV) is defined after preliminary palpation of the apical impulse, usually in the V intercostal space, moving from anterior axillary line towards the heart. Normally it situated medial to the midclavicular line for 1-2 cm. The upper border of relative cardiac dullness , formed by auricle of left atrium and pulmonary artery trunk is defined by percussing from top to bottom, 1 cm lateral from left sternal line (but not along left para-sternal line!). Normally it situated at the III rib level.

absolute (total) cardiac dullness The right border of relative The left border of relative cardiac dullness cardiac dullness

Fig.6. The relative and absolute (total) cardiac dullness borders

Normal borders of the absolute cardiac dullness: right - in the IV intercostal space along the left edge of the sternum, the upper - level of the lower edge IV R. at the left parasternal line, left - 1-2 cm medially from the left border of relative cardiac dullness. Changes of heart dullness borders may be caused by extra cardiac reasons. So, while high diaphragm level heart takes a horizontal position that leads to increasing of the transverse heart size. At low diaphragm level heart takes a vertical position, and, accordingly, its transverse size becomes less. Pleural fluid or free pleural air in one of the pleural cavities brings to displacing of .the cardiac dullness borders to the healthy side, atelectasis or lung shrinking, fibro thorax – to the sore side. Area of superficial cardiac dullness sharply decreases or disappears at the emphysema and increases at the lung shrinking. Increase of superficial cardiac dullness area also occurs in heart ante displacement by mediastinal tumour, pericardium effusion, right ventricle dilation.

Relative cardiac dullness borders are displaced because of the heart chambers dilation. Relative dullness borders displacement to the right is caused by right atrium and right ventricle dilation. Relative dullness is displaced upwards because of left atrium and pulmonary artery trunk dilation. Relative dullness borders displacement to the left is the result of left ventricle dilation. It is necessary to remember, that sharply dilated and hypertrophied right ventricle shoving back the left ventricle also can displace relative dullness border to the left. Aortic dilation leads to dullness diameter increase in the 2nd intercostal space. Measurement of heart diameter. For measurement of heart diameter the distances from right and left borders of relative cardiac dullness to midsternal line are defined. Normally these distances make respectively 3-4 cm and 8-9 cm, and heart diameter makes 11-13 cm (Fig.7).

Fig.7. Measurement of heart diameter. Defining of vascular bundle borders . The vascular bundle including aorta, vena cava superior and pulmonary artery is not simple to percuss. Soft percussion is applied, moving vertically placed pleximeter finger along the II intercostal space on the right and on the left towards the sternum. Normally vascular bundle borders coincide with right and left edges of the sternum, its width doesn't exceed 5-6 cm (Fig.8). 18

Fig.8. Defining of vascular bundle borders Defining of heart configuration. For defining of heart configuration the borders of right and left contours of relative cardiac dullness are additionally defined by percussing in the right III intercostal space and in the left III and IV intercostal spaces. Having connected all the points corresponding the borders of relative cardiac dullness, one can obtain the idea about heart configuration. Normally an obtuse angle is clearly defined along the left heart contour between the vascular bundle and the left ventricle - the so- called waist of the heart. The arc of the right contour of the heart in norm –vena cava superior– on the edge of the sternum to R. III, right atrium in the 3-4 intercostal spaces 1 cm outwards from the right edge of the sternum. The angles of the right contour of the heart in norm – angle between vena cava superior and right atrium and between the right atrium and diaphragm in the 5 intercostal space from the sternum. The arc of the left contour of the heart in norm - I intercostal space at the edge of the sternum - aortic arch, II intercostal space at the sternum – the arc of the pulmonary artery, level III R. over the edge of the sternum arc of the left atrium, below the arc of the left ventricle. The "waist" of the heart is the angle between the vascular bundle and the arc of the left ventricle. The vertex of this angle- left atrium auricle . With the increase of LP waist heart "smoothed", while increasing the LV – "stressed". 19

Mitral configuration I - waist heart smoothed at the expense of hypertrophy of the left atrium, the vascular bundle can be extended due to the dilatation the pulmonary artery, it is possible to laterally shift the right border of relative cardiac dullness due to right ventricle hypertrophy with the development of pulmonary hypertension; the reason for the configuration is mitral stenosis. Hemodynamics abnormalities in mitral stenosis In compensation stage of disease: the area of mitral ostium is significantly less than normal (4-6 cm2), that leads to left atrium repletion with blood. This blood had not time to move to the left ventricle, and there is also blood, arrived from pulmonary veins. It results in left atrium hypertrophy. In decompensation stage of disease: left atrium contractility is decreased, pressure within it increases, that leads to the pressure rise within the pulmonary veins and pulmonary capillaries. The latter leads to switching on Kitaev's reflex – the pressure rise within the pulmonary veins ostii causes the narrowing of the pulmonary arterioles- and when pressure rising within the pulmonary artery and further overload and hypertrophy of the right ventricle. The left ventricle diminishes at the rate because it performs the less work (Application Fig.4). Mitral configuration II - the reason for the configuration is mitral incompetence. Mitral valve incompetence (insufficientia valvulae mitralis ) appears in that cases when mitral valve on left ventricle systole incompletely closes left atrioventricular ostium and blood regurgitates from the ventricle to the atrium. Mitral incompetence may be organic and functional. Organic mitral incompetence more frequently appears as a result of rheumatic endocarditis due to which connective tissue develops in valve leaflets and later on it is wrinkled and causes shortening of leaflets and attached chordae tendinae. As a result of these changes valve edges during systole closes incompletely, forming a chink through which in ventricle contraction the part of blood regurgitates into the left atrium. Rarely wrinkling of valve leaflets and shortening of chordae tendinae develops as a result of atherosclerosis.

In functional or relative mitral incompetence mitral valve is not changed but its ostium is enlarged and valve leaflets close it incompletely. Relative incompetence may develop owing to left ventricle dilatation in myocarditis, myocardidystrophy, myocardiosclerosis, when circular muscle fibers, forming muscle ring around the atrioventricular ostium weaken, and also in papillary muscles damage. Hemodynamics abnormalities Hemodynamics in mitral incompetence is characterized by partial blood regurgitation into the left atrium in incomplete closure of mitral valve leaflets. The atrium filling increases since the regurgitated part of blood adds to usual blood volume, arrived from pulmonary veins. Pressure in the left atrium increases, it dilates and hypertrophies. During diastole greater than normal blood volume flows from overfilled left atrium into the left ventricle, that leads to left ventricle overfilling and dilatation. Left ventricle should work with overload, due to which its hypertrophy develops. Overwork of hypertrophied left atrium and left ventricle protractedly compensates possessed mitral incompetence (Application Fig. 1-3). In decrease of hypertrophied left atrium contractile capacity congestive phenomena in lesser circulation circle appear and pressure rises, that demands overwork of right ventricle. So in time in mitral incompetence the right ventricle hypertrophy may develop. On the heart percussion its dullness enlargement to the left and upwards due to left atrium and left ventricle dilatation is revealed. The heart acquires mitral configuration with smoothed cardiac waist. On right ventricle hypertrophy cardiac dullness also shifts to the right (Fig. 8,9).

Fig.8. Radiography of the chest in combined heart defect shows mitral configuration of the heart.

Fig.9. M itral configuration II of the heart.

Aortic heart configuration – the reasons of this configuration are stenosis of aortic ostium and aortic incompetence , arterial hypertension.

Stenosis of aortic ostium (aortic stenosis, stenosis ostii aortae ) creates difficulty for blood ejection into aorta on the left ventricle contraction. Acquired aortic valve stenosis often results from progressive degeneration and calcification of a congenitally bicuspid valve. Rheumatic fever, bacterial endocarditis and arteriosclerotic degeneration are rarer causes. This valve disease appears owing to adhesion of valve cusps or fibrous narrowing of aortic orifice. Hemodynamics abnormalities A little narrowing of aortic orifice doesn’t cause significant circulation alteration. If the degree of stenosis is high, during systole the left ventricle empties incompletely, as all blood volume has no time to pass across narrow orifice into aorta. On diastole normal blood volume from the left atrium adds to this residual blood portion, that leads to left ventricle overfilling and pressure rising within it. This abnormality of intracardiac hemodynamics is compensated by left ventricle overwork, and causes its hypertrophy (Application Fig.7) On percussion the displacement of relative dullness borders to the left and aortic heart configuration (with accentuated cardiac waist), caused by left ventricular hypertrophy are detected (Fig.10,11).

Fig.10. Aortic heart configuration.

Fig.11. Radiography of the ches t in aortic incompetence shows typical aortic configuration of the heart. Aortic incompetence ( insufficientia valvulae aortae ) is valve disease in which the semilunar cusps close incompletely the aortic orifice and during diastole blood regurgitates from a orta into left ventricle. Aortic regurgitation occurs if the aortic valve ring dilates, as a result of dissecting aneurysm, ankylosing spondylitis or syphilis for example, or if the valve cusps degenerate, such as after rheumatic fever, atherosclerotic lesion or endocarditis. Anatomical changes depend on etiology of aortic lesion. After rheumatic fever inflammatory-sclerotic process at the base of valvular cusps leads to their wrinkling and shortening. In syphilis and atherosclerosis pathologic process may affect only aorta itself, causing its dilatation and taking -up of valvular cusps without their affecting, or connective tissue expands on valvular cusps and deforms them. In sepsis ulcerous endocarditis leads to destruction of valve parts, defects forming in the cusps and their subsequent scarring and shortening. Hemodynamics abnormalities In aortic incompetence during diastole blood comes in the left ventricle not only from left atrium but regurgitates from aorta too. It causes left ventricle overfilling and

24 stretching on diastole. During systole left ventricle contracts with grater force t o eject into aorta increased stroke volume. Left ventricle overwork leads to its hypertrophy, and increase of systolic blood volume in aort a causes its dilatation . Sharp fluctuation of blood pressure within aorta during systole and diastole is characteris tic for aortic incompetence. Increased as compared with normal blood volume within aorta during systole causes increase of systolic blood pressure, and as a part of blood volume regurgitates into ventricle during diastole, diastolic pressure rapidly declin e (Application Fig.5 -6). "Trapezoidal" configuration of the heart - the heart has a trapezoid shape, waist of the heart, angle between vena cava superior and right atrium and angle between right atrium and diaphragm "disappear ", the reason of configuration is hydropericardium (Fig.12).

Fig.12 "Trapezoidal" configuration of the heart. " Spherical” configuration of the heart when the ventricular septal defect due to the discharge of blood from the left to the right ventricle.

Fig.13"Spherical” configuration of the heart. in a patient with a congenital heart defect. The chest radiograph of a patient with a ventricular septal defect (direct view): the shadow of the heart increased at the expense of both ventricles, visible bulging arc pulmonary trunk (arrow), pulmonary picture in the basal parts of the lungs are strengthened.

"Drip" configuration of the heart - the left and right border of cardiac dullness is shifted medially, the area of cardiac dullness is diminished, the heart becomes "drip" form, cause - emphysema of the lungs (Fig.14).

Fig.14. "Drip" configuration of the heart

"Cor bovinum" ("bull" heart) - the area of cardiac dullness is increased by hypertrophy and/or dilatation of its main offices in cardiomyopathy, advanced forms of heart failure.

Fig.15. "Cor bovinum"

Auscultation of the heart and blood vessels.

Auscultation points of the heart valves do not coincide with the projection places of the valves on the anterior chest wall (only pulmonic valve auscultation point practically coincides with the projection of the pulmonary artery valve).

Places of three heart valves projection - pulmonary, aortic and mitral - are located very close to each other, about the place of the III rib attachment to the sternum (therefore to distinguish particular sounds associated with damage of each of these valves, when listening to their places of projection is not possible). The diameter of the valves openings is large enough and is 2-3 cm for pulmonary, aortic and mitral valves and 3-6 cm for tricuspid valve. Therefore, in determining the projection of the heart valves it must be taken into account their length, as projection of the valve is not the point, but rather the line of few centimeters. The surface projections of the heart valves on the anterior chest wall (approximately) are as follows (Fig. 16): 1. The pulmonic valve is located at the place of attachment of the upper edge of III left costal cartilage to the sternum (1/2 portion of the valve is located behind the rib cartilage, 1/2 part of the valve-behind the sternum). 2. Aortic valve is located just medially, slightly lower and deeper than pulmonary valve - almost in the middle of the sternum at the level of the III mid-rib. Bicuspid (mitral) and tricuspid atrioventricular valves are located behind the sternum in the arcuate line connecting places of the lower part of the left III rib cartilage and the right V-VI costal cartilages attachments to the sternum. 3. Bicuspid (mitral) valve is located within the limits of upper third of this line and is located in between the attachment place of the lower edge of the III rib cartilage to the sternum and the level of the third left intercostal space. 4. Tricuspid valve is within the limits of lower 2/3 of this line and is located in between the level of the left third intercostal space and the attachment point of the right V costal cartilage to the sternum (in fact, in the lower part of the sternum body).

Fig. 16. Projection of the heart valves on the anterior chest wall and their auscultation points Since all the heart valves are located close to each other, to evaluate the sound effects associated with the work of each valve there are used more remote points from the valves location, where the sound is carried either by the flow of blood, or by myocardium of the heart area, where this sound is produced and where the summation of the sounds originating in neighboring parts of the heart is minimal. There are distinguished the 6 heart auscultation points: 4 main and 1 additional points. «Assignment» numbers to the auscultation points (1st auscultation point, 2nd auscultation point, etc.) and listening to the heart valves in this sequence in clinical practice is determined by the frequency of their damage (i.e. the most frequently damaged mitral valve, and most rarely - tricuspid one). 1. The first auscultation point - region of the apical impulse (normally - the V intercostal space slightly medially from l. medioclavicularis sinistrum, in the pathology, apical impulse may be displaced considerably from its location in the norm). At this point, mitral (bicuspid) valve is well heard. This is because in its projection (behind sternum at the level of the lower edge of the III rib cartilage - 3rd intercostal space) mitral valve is rather deeply spaced apart from the chest wall (i.e. the sounds from it are not properly 29 heard), and at the apex of the heart, which is formed by the left ventricle, mitral valve sounds are well conducted by dense heart muscle. 2. The second auscultation point -2nd right intercostal space close to the sternum. This point is a place of the aortic valve auscultation. As mentioned above, the aortic valve is projected on mid-sternum at the level of the III rib middle, but it is common to listen to the aorta in the right 2nd intercostal space, because aorta here comes close to the anterior chest wall and here aortic valve sounds are well conducted along by the flow of blood and the wall of the aorta.Therefore, when listening to the right 2nd intercostal space, one can be sure that the sounds and murmurs belong exactly to the aortic valve. 3. The third auscultation point - 2nd left intercostal space close to the sternum. This point is very close to the projection of the pulmonic valve (attachment of upper edge of the III costal cartilage to the sternum). Pulmonary artery valve is listened here. 4. The fourth auscultation point - on the sternum near the xiphoid process. The fourth auscultation point is somewhat lower than the projection of the tricuspid valve and is located near the site of processus xifoideus attachment to the sternum - at the lower part of the sternum to the right. 4 point is a tricuspid valve auscultation point. 5. Fifth (extra) auscultation point - 2/3 of the stethoscope should be put in the left 3rd intercostal space close to the sternum, and 1/3 - on the sternum. This is so-called Botkin-Erb's point 1. Aortic valve is listened here. Currently, auscultation of the heart only in the 5 fixed auscultation points is considered insufficient. According to M.M. Mirrahimov et al. (1981), «the selection of these points is useful when teaching students at the beginning, because it «ties» to each other regions of valve localization and the most frequent place of its auscultation on the anterior chest wall. But for the physician the heart auscultation in the standard points is insufficient due to the fact that the murmurs usually (with rare exceptions) do not cover the point, but the region. At this auscultation point the murmur can only be heard or conducted, and its maximum can be placed between the points. Meanwhile, in the majority of cases, it is possible to assess the murmur properly only in the region of its maximum sounding. This implies that one needs to listen to the entire area of the heart».

In any case, the stethoscope must be moved step-by-step slowly from area to area to «not to omit» any important finding in the presence of pathology, while listening to the heart. The heart auscultation: heart sounds abnormalities Phase of ventricular systole is the asynchronous contraction, isovolumic (isometric) contraction, the exile (fast and slow). Phase of diastole ventricular – izovolemic reduction, quick blood circulation, slow blood circulation. I tone – systolic, consists of: a) the valve component vibrations of the valves atrioventricular valves in the phase izovolemic reduction. b) muscular component – vibration of ventricular myocardium in the phase izovolemic reduction. C) the vascular component of oscillations of the initial segment of the aorta and pulmonary trunk in tension with their blood during the exile II tone – diastolic, comprises: a) the valve component vibrations of the valves the semilunar valves of the aorta and the pulmonary trunk when closed in early diastole b) the vascular component oscillations of the walls of the aorta and the pulmonary trunk at the beginning of diastole. The aortic component is almost always normal and disease precedes pulmonary, because aortic valve closes slightly before the valve LA. III tone – vibrations during rapid passive filling of the ventricles with blood from the Atria during diastole (using a 0.12-0.15 from the beginning of the II tone) The IV tone is ventricular filling in late diastole due to active contraction of Atria. III and IV the normal tones are heard only in children and young lean people, especially on the left side, clearly recorded on the FCG. Identification of III and IV tones from middle aged persons and the elderly – pathology.

In clinical practice the following changes of heart sounds may be met: 31

1. Volume change of the main sounds (S1 and S2); 2. Splitting (doubling) of the main sounds; 3. Appearing of additional sounds: S3 and S4, mitral valve opening snap (OS), additional systolic sound (click) and the so-called pericardium tone. Diminished first heart sound. The first heart sound may be diminished by the following reasons: 1. incomplete closure of atrioventricular valves (for example, in mitral or tricuspid incompetence), 2. sharp slowing down of ventricle contraction and increase of intraventricular pressure due to myocardial contractile capacity decrease in patients with cardiac insufficiency and acute myocardial lesion. 3. significant slowing down of hypertrophic ventricle contraction, for example, in aortic stenosis; 4. unusual position of atrioventricular valves cusps just before the beginning of isovolumetric ventricular contraction.

Accentuating of S1. There exist two main reasons of accentuating of S1: 1. increase of isovolumetric ventricular contraction rate for example, in tachycardia or thyrotoxicosis, when the rate of all the metabolic processes in the organism, including myocardium, is increased; 2. consolidation of cardiac structures taking part in vibrations and formation of the first sound, for example, in mitral stenosis.

Diminished S2. The main reasons of the second heart sound diminishing are: 1. non-hermetic closure of aortic and pulmonary artery semilunar valves; 2. decreased rate of semilunar valves closure in: a. heart failure accompanied by decreased rate of ventricles rela-xation; b. arterial pressure decrease; 3. adhesion and decrease of motility of semilunar valves cusps, for example, in valvular aortic stenosis. 32

Accentuating S2 Enhancing (accent) of the second heart sound on aorta may be caused by: 1. arterial pressure increase of various genesis (due to inc rease of aortic valve cusps shutting rate); 2. consolidation of aortic valve cusps and aortic walls (atherosclerosis, syphilitic aortitis, etc).

Main reason of S1 splitting is asynchronous closure and vibrations of mitral (M) and tricuspid (T) valves. Su ch situation may appear, for example, in case of the right bundle branch block Doubling and splitting of S2 are, as a rule, associated with increase of blood ejection time of the right ventricle and/or decrease of blood ejection time of the left ventricle that leads, respectively, to later appearance of pulmonary component and/or earlier appearance of aortic component of S2 (Fig. 17 .).

nd Fig. 17. Physiologic splitting of S 2 can usually be detected in the 2 left interspace.

The pulmonic component of S 2 is usually too faint to be heard at the apex or aortic area, where S 2 is single and derived from aortic valve closure alone.

Any change of diastolic ventricular myocardial tonus, rate of its relaxation or increase of atrium volume may lead to appearance of pathologic third heart sound, or protodiastolic gallop rhythm (Fig.18).

Fig. 18. Third heart sound occurs early in diastole during rapid ventricular filling. It is later than an opening snap, dull and low in pitch, and heard best at the apex in the left lateral decubitus position. The bell of the stethoscope should be used with very light pressure.

The fourth heart sound (S 4) (presystolic) may be heard in systemic hy pertension and in idiopathic hy pertrophic subaortic stenosis. It has been attributed to sudden ventricular distention associated with an augmented left atrial contraction and increased left ventricular end-diastolic stretch (Fig. 19 ). In healthy people physiologic fourth sound is very soft, low frequent and is found rather rarely, predomin antly in children and teenagers. Pathologic accentuation of S4 in adults is named as pre -systolic gallop rhythm.

Fig. 19. Fourth heart sound is an atrial contraction sound that occurs in late diastole, preceding S 1. S 4 has a dull, low pitch, and heard better with the bell.

The third or fourth heart sounds may be heard in rapid succession with first and second heart sounds (triple rhythm), when the heart rate is fast. The cadence so produced has been likened to a horse's gallop, and is called gallop of the third (Lup De -da, Lup De-

34 da) or forth heart sound (De La-lup, De La-lup). A gallop or triple rhythm of the third heart sound may be heard in young healthy subjects after exercise. It is an important sign of heart failure from any cause, and it almost always arises from rapidly filling left ventricle. A gallop of the fourth heart sound, unlike that of the third sound, is not a sign of failure but of compensation. A gallop of all four heart sounds (summation gallop) is sometimes heard in heart failure. Summation gallop is a three-part ventricular rhythm when, in result of sharp shortening of slow filling phase in presence of tachycardia pathologic S3 and S4 merge into one additional sound. Aortic ejection click is a sharp, brief, high-pitched sound, which occurs soon after the first heart sound (after the closure of the aortic valve). It is best heard in expiration over the aortic area and the apex. It is associated with dilatation of the aorta and can be heard in cases of hypertension, coarctation and atherosclerosis. Systolic gallop is a three-part rhythm appearing in case of additional short sound, or systolic flap, rise in the period of ventricles systole (between S1 and S2). A nonejection systolic click is heard together with a systolic murmur in association with mitral valve prolapse. The mitral valve leaflets do not coapt during systole; the posterior cusp prolapses, sometimes indicated by a click, and the ensuing murmur is caused by regurgitation of blood into the left atrium. In various manuals rhythm of quail is called «quail rhythm». Mitral valve opening snap (OS) appears exclusively in case of mitral stenosis at the moment of mitral valve cusps opening. In fact, such sounds are emitted by quail. Quail (Latin Coturnix coturnix) is a bird, subfamily partridge, galliformes class (Boehme R.L, V.E. Flint, 1994). «Male sings, the female brings out nestlings, so it is quiet, not showing her nest. Experts claim that not all quails sing the same. They, like humans, have different tone and voice power. Some have clean, loud one, and are heard a mile away, while others are more gentle and pleasant» (Isachenko L. Science and Life, 2006. - № 1).

The heart auscultation: heart murmurs Cardiac murmurs are relatively long lasting sounds appearing during turbulent blood motion. The turbulence appears in case of disturbance of three hemodynamic parameters normal proportion: 1. Diameter of valve ostium or vessel lumen; 2. Blood flow velocity (linear or volume); 3. Blood viscosity. Murmurs heard above the region of the heart and large vessels are divided into intra- and extracardiac. Intracardiac murmurs. Intracardiac murmurs are divided into: 1. organic, appearing due to rough organic lesion of valves and other cardiac anatomic structures (interventricular or interatrial septum); 2. functional murmurs based not on rough anatomic structures lesions, but on lesion of valvular functions, blood flow acceleration through anatomically unchanged ostiae or blood viscosity decrease. Organic murmurs: all the organic intracardiac murmurs appear in presence of narrowing, dilation or other obstacles, for example, parietal thrombus or atherosclerotic patch on aortic wall in cardiac cavities or initial parts of main vessels. One should give its detailed characteristic, namely, define: 1. murmur relation to cardiac activity phases (systolic, diastolic, etc.) (Fig. 20, 21); 2. region of maximal murmur intensity; 3. murmur transmission; 4. timbre, volume of the murmur; 5. shape of murmur. For more information look at tables 3,4

Fig. 20. Main types of systolic murmurs.

Fig. 21. Main types of diastolic murmurs.

Table 3.

Chief systolic murmurs

Time and quality Accompanying signs Interpretation 1. Ejection, harsh midsystolic Slow rising pulse, low systolic pressure, Aortic stenosis accentuation or prolonged heaving apex beat, systolic thrill, ejection click,

soft or absent A 2 2. Ejection, as above. Loudest Jerky pulse, atrial impulse over apex, lifting Hype rtrophic obstructive in left 3 rd , 4 th interspace apex beat cardiomyopathy 3. Ejection, as above Hyperkinetic states, aortic incompetence, Increased flow complete heart block 4. Ejection, as above No signs Aortic stenosis 5. Ejection, over pulmonary Increases during inspiration Pulmonary stenosis area 6. Ejection, short, over Hyperkinetic states, left-to-right shunt (ASD, Increased flow pulmonary area VSD) 7. Late ejection, over mitral Mid-systolic click Mitral valve prolapse area 8. Pansystolic, blowing, Large volume pulse, displaced and vigorous Mitral incompetence mostly uniform apex, right ventricular heave, S 3, louder during expiration 9. Pansystolic, as above. Best As above plus thrill frequently presents Ventricular septal defect heard over left 3 rd , (VSD) 4th interspace

Table 4.

Chief diastolic murmurs

Time and quality Accompanying signs Interpretation 1. Early diastolic, high-Collapsing pulse, Corrigan's sign, wide Aortic incompetence pitched, blowing pulse pressure, displaced and vigorous apex 2. Early diastolic, a short, Prominent 'a' wave, right ventricular heave, Graham Steell murmur high-pitched whiff loud P 2 (functional pulmonary incompetence) 3. Mid-diastolic, rough, Malar flush, small volume pulse, tapping Mitral stenosis rumbling impulse, right ventricular heave, opening snap 4. Mid-diastolic, short, Signs of mitral incompetence, VSD or Inflow (mitral) murmur

38 following S 3 patent ductus 5. Mid-diastolic, short, Signs of atrial septal defect (ASD) Inflow (tricuspid) murmur over tricuspid area 6. Continuous systolic and Collapsing pulse, thrill, mitral inflow Patent ductus, aortopulmonary diastolic, machinery noise murmur septal defect

Examples of most characteristic murmurs in five acquired cardiac defects: mitral incompetence, mitral stenosis, aortic stenosis, tricuspid incompetence.

Mitral incompetence is characterized by diminished S1, systolic murmur appearance and S2 accent at the pulmonary artery. On PhonoCG decrease of S1 amplitude is marked in significant mitral incompetence due to falling out of S1 valvular component and overfilling of left ventr icle. Minor degree of mitral incompetence isn't accompanied by S1 diminishing. The most important in mitral incompetence diagnostics is a presence of systolic murmur with maximal intensity at the apex (Application Fig.2 ). In severe valve disease murmur of considerable intensity is registered at the left axilla. Systolic murmur is directly connected with defect, formed between valve leaflets and reverse blood flow (regurgitation) through this chink. Murmur in mitral incompetence begins directly after S1 and has decrescent character. It may occupy all systole (pansystolic) or part of systole according to the degree of mitral incompetence. Murmur amplitude is more when the defect is pronounced (Fig. 2 2).

Fig. 22. When the mitral valve fails to close fully in systole, blood regurgitates from left ventricle to left atrium, causing a murmur. S 1 is often decreased. An apical S 3 reflects the volume overload on the left ventricle.

At the pulmonary artery increase of S2 pulmonary component (P2) is noticed, S2 is frequently splitted.

Mitral stenosis : Since a little amount of blood gets into left ventricle and it contracts fast, so S1 at the apex becomes loud, flapping. Here after S2 the additional heart sound – mitral opening snap – is listened. Flapping S1, S2 an d opening snap (OS) create the typical of mitral stenosis melody called ―quail rhythm (Fig.23). A rumbling diastolic murmur at the apex is typical of mitral stenosis, because there is narrowing down blood flow from the left atrium to the left ventricle on diastole (Application Fig.1 ). This murmur may occur in the very beginning of diastole, i.e. to be protodiastolic, because due to pressure gradient in atrium and ventricle the blood flow velocity will be higher at the diastole beginning. However, murmur app ears only at the end of diastole before the very systole – presystolic murmur, which appears in blood flow acceleration at the end of diastole due to atrial contraction. There may be presystolic accentuation and the murmur may be preceded by an opening sna p. Exercise and positioning the patient in the left lateral position will accentuate the murmur (Fig.22).

Fig. 23. When the leaflets of the mitral valve thicken, stiffen, and become distorted, the valve fails to open sufficiently in diastole. The resulting murmur has two components: mid-diastolic (during rapid ventricular filling), and presystolic (during atrial contraction).

S1 is accentuated. An opening snap (OS) often follows S 2 and initiates the murmur. As pulmonary hypertension develops, the pulmonary second sound becomes accentuated.

Aortic incompetence: on auscultation diminished S1 at the apex is revealed, because during systole there is no period of closed valves. S2 at the aorta is also diminished , and 40 in significant cusps destruction it may not to be heard. In syphilitic and atherosclerotic lesion of aorta S2 may be clear enough. The typical auscultative sign of aortic incompetence is diastolic murmur, listened at the aorta and at the Botkin-Erb' s point, which is best heard by sitting the patient upright, leaning forward in full expiration. It usually is soft, blowing protodiastolic murmur, weakening to the end of diastole as blood pressure decreasing in aorta and blood flow slowing (Application Fig.4, Fig . 24).

Fig. 24. Diastolic murmur in aortic regurgitation is located at the 2 nd - 4th left interspaces and radiates to the apex, to the right sternal border. The murmur is high - pitched, blowing in quality, may be mistaken for breath sounds. It is heard best with the patient sitting, leaning forward, with breath held in exhalation. In aortic incompetence at the apex murmurs of functional origin may be also heard. So, in large left ventricular dilatation relative mitral incompetence occurs and sy stolic murmur at the apex appears. Rarely diastolic (presystolic) murmur - Flint's murmur appears due to mitral valve cusps raising by a strong stream of blood regurgitating during diastole from aorta to left ventricle. It results in difficult blood flow f rom LA to LV during active atrium systole. Sometimes in this valve disease two sounds (Traube's doubling sound) and the Vinogradov -Duroziez‘s doubling murmur heard over the femoral artery are revealed. They are explained by vibration of arterial wall on sy stole and diastole during pulse wave passing.

Aortic stenosis: on the heart auscultation at the apex diminished S1, connected with left ventricle overfilling and lengthening of its systole, is listened. At the aorta S2 is diminished, in case of adhered val ve cusps immobility it may not be heard. Rough systolic murmur, connected with blood flow across the narrow orifice, at the aorta is 41 characteristic. It radiates along blood flow direction to the carotids, and sometimes it may be heard at the interscapular area (Application Fig.7, Fig. 25).

Fig. 25. Midsystolic murmur in aortic stenosis is heard in the 2 nd right intercostal space, radiates often to the neck and down the left sternal border, even to the apex. Heard best with the patient sitting and leaning forward. A 2 decreases as the stenosis worsens. Although examination of the alimentary and respiratory systems forms part of the complete clinical as sessment, palpation of the abdomen for hepatomegaly, firm pressure over the sacrum for dependent oedema, an d auscultation over the lung bases are important for the clinical evaluation of the cardiovascular system. Functional murmurs a ll the functional murmurs are conditionally divided into three groups: 1. dynamic murmurs, based on significant blood flow velocity increase in absence of any organic cardiac diseases (for example, dynamic murmurs in thyrotoxicosis, cardiac neurosis, febrile conditions). 2. anemic murmurs, caused by decrease of blood viscosi ty and certain blood flow acceleration in patients with anemias of different genesis; 3. murmurs of relative valvular incompetence or relative narrowing of valvular openings caused by various valvular function lesions, including patients with organic card iac diseases. Extracardiac murmurs Pleuropericardial (pleural extrapericardial) rub occurs when the inflammation process captures part of the pleura, close to the heart, and simultaneously the external pericardial layer. This murmur is heard not only in the respiratory phases, but is synchronic with the heartbeats. To distinguish it from the true pericardial rub caused by

42 friction of the inflamed pericardium layers, their attitude to breathing serves. While in true pericarditis friction rub is best heard at breath holding, pleuropericardial rub is best heard at inhalation, sometimes at exhalation, because under these conditions, larger pleural layers surfaces contact with each other (Pletnev D.D., 1928).

Cardiopulmonary murmurs occur in adjacent to the heart parts of the lungs, expanding during systole due to the reduced heart volume. Air penetrating into these parts of the lungs, gives murmur, vesicular in nature («vesicular breath-ing») and systolic in time [«vesicular breathing» with the heart rate] (Chernorutsky M.V., 1954).

Auscultation of vessels Vinogradov-Durozier's murmur (Vinogradov N.A., 1831-1885, Russian clinician; Durozier Paul Louis, 1826-1897, French physician) is a combination of systolic and diastolic murmurs detected by pressing a stethoscope on the projection area of the femoral artery; it occurs in aortic insufficiency due to reciprocating blood flow through the major arteries. Murmurs are not heard in a healthy person in ordinary peripheral arteries auscultation. If stethoscope slightly presses on the carotid, subclavian, brachial or femoral arteries, murmur of stenotic origin may appear during their auscultation. In aortic insufficiency, during auscultation of the femoral artery with a little pressure of stethoscope on it, two murmurs (Vinogradov-Durozier's double murmur) are heard instead of one that can be heard in the normal condition. «First» murmur is caused by artificial narrowing of the arteries, «second» - by the reverse blood flow. Traube's dual sound (Traube L., 1818-1876, German physician) - auscul-tatory phenomenon: double sound which is heard over the femoral artery. The appearance of Traube's dual sound is a sign of the aortic valve insufficiency. Two sounds can be heard on auscultation of the carotid and subclavian arteries, one sound is heard on auscultation of the femoral artery, no sound is heard over the brachial artery normally in a healthy person. First sound is quiet, connected with the sudden strain of the arterial wall during admission of blood wave. Second sound (diastolic) is the usual

II heart sound, heard on auscultation of the heart and caused by slamming of the aortic valve, but held by the blood flow to the carotid and subclavian arteries. In case of aortic insufficiency over femoral artery instead of normal one audible sound there two loud sounds are identified, similar to the sound of gun shots (Traube's dual sound).The first sound is caused by the sudden tension of the arterial wall during admission of blood wave, and the second is due to its sudden relaxation because of sharp decrease in blood supply of the femoral artery caused by blood regurgitation into the left ventricle. One should remember, that in aortic insufficiency classic II heart sound disappears and heard over the femoral artery sound is not the II heart sound, held here, but an independent sound, emerging in the femoral artery itself. It should be kept in mind that both Traube's dual sound, and Vinogradov-Duroziez's dual murmur can be observed not only in aortic insufficiency, but also in infectious diseases, Graves' disease and severe anemia, apparently due to the lowering of the arterial walls tonus (Gubergrits A.J., 1956).

Techniques for improving the auscultation Sirotinin-Kukoverov's sign (Sirotinin V.N, 1855-1936, Russian therapist; Kukoverov N.G. - assistant doctor of Sirotinin clinic) is appearance (or enhancement in its presence) of systolic murmur at the point of aortic valve auscultation with the patient's raised hands (e.g., at the location of the hands on the hind head). This is the sign of atherosclerotic lesion of ascending thoracic aorta. Rivero Carvallo sign (Rivero Carvallo J.M.R.) - pathophysiological phenomenon: enhancement of auscultation phenomena (mainly systolic murmur), related to the activities of the right heart, with breath holding during or at the height of a deep inhalation, helps to identify defects of the tricuspid valve. In some guidelines there is error in naming the symptom, it is written incorrectly «Rivero-Carvallo sign». J.M.R. Carvallo was Mexican doctor working at the National Heart Institute in Mexico City. This sign he described in 1946. According to S. Mangione (2004), «medical folklore attributed to him partner (Dr. Rivero), so the sign is often named Rivero-Carvallo sign. In fact, Rivero is one of Carvallo's names. 44

Palpation of the radial pulse Feeling the right radial pulse has been by tradition the first invasion of a patient's person by his physician. This first contact should therefore transmit warmth, confidence and reassurance. If your hands are cold you should rub them vigorously to warm them. Hold the patient's hand firmly in one hand and feel the pulse with the fingers of the other hand. The first important issue to settle is whether the pulse is present and palpable or absent due to any local or generalized vascular disease. Next, you need to answer questions about four features of the pulse (Table 5). The first two of these are comparatively easy and can be answered by counting the pulse rate at least 30 seconds. This is long enough to form an initial opinion about the rhythm, whether regular or irregular due to ectopic beats or completely chaotic as in atrial fibrillation. Table 5. Examination of the pulse Feature Interpretation Rate Resting, 60-80 beats per minute -1 Tachycardia, 90 or more beats per minute - 1 Bradycardia, 60 or less beats per minute -1 Rhythm Regular Irregular - ectopic beats or atrial fibrillation Chaotic - atrial fibrillation Volume Normal Large - hypertension, diastolic overload Small - low output states Character Normal Collapsing - aortic incompetence Slow rising - aortic stenosis Bisferiens - aortic stenosis and incompetence

Volume. This is the upstroke of the pulse wave as appreciated by the pulps of the examining fingers, and reflects the pulse pressure or the difference between the systolic and diastolic pressures. It gives some idea about the diastolic burden, output and contractility of the left ventricle. A great deal of experience is required to decide whether

45 a particular pulse volume is normal, small or large. It is advisable to feel your own pulse simultaneously and develop a habit of making a decision about the volume of the patient's pulse. A large volume pulse suggests hypertension or diastolic overload (e.g. aortic or mitral incompetence, patent ductus arteriosus, severe anaemia, fever, thyro-toxicosis, etc.). A small volume pulse is usually associated with low output states such as mitral or aortic stenosis and any condition with blood pressure. Character. The character of a pulse is the entire waveform as felt by the examining fingers. This is better appreciated by feeling the brachial pulse with the thumb; the arm of the patient should be kept straight and your thumb should gently press the artery against the bone until the entire upstroke is absorbed into the pulp of the thumb. This method should be practiced as it can be quite useful in detecting the slow rising.pulse of aortic stenosis, and bisferiens pulse of mixed aortic valve disease and severe aortic incompetence. An exaggerated upstroke, or a bounding pulse, may be felt in patients with elevated stroke output (mitral regurgitation, ventricular septal defect, high fever), sympathetic overactivity (thyrotoxicosis), and in patients with rigid, sclerotic aorta. A slow upstroke (pulsus tardus) is felt in cases of left ventricular outflow obstruction, and may be associated with a thrill felt over the carotids (carotid shudder). A large volume pulse may have a collapsing character which can be detected by lifting the arm of the patient, with the four fingers of your one hand placed firmly on his wrist, and the palm of your other handplaced over the brachial artery. A collapsing (Corrigan's) pulse will impart a flick across your fingers on both hands, and suggests a large upstroke (due to diastolic overload) and quick downstroke due to a runoff either at the aorta valve (aortic incompetence) or from the aorta into the left pulmonary artery (patent ductus arteriosus). It is the change of character on lifting the arm and not simply its easy palpability that is specific to a collapsing pulse. Corrigan's pulse can be seen and felt in the neck over the carotid artery. Pulsus bisferiens with two peaks (the tidal and percussion waves) can be felt over the carotids, but it is best felt over the peripheral pulses such as the radials, brachials and 46 femoralis in some patients with combined aortic valve disease and severe aortic regurgitation. Pulsus alternans (equally spaced and alternating large and small beats) is a sign of left ventricular depression. It must be distinguished from pulsus bigeminus in which a premature ventricular beat occurs after every normal beat. This ectopic beat feels weak at the wrist and is easily confused with the weak beat of pulsus alternans, but in the latter the rhythm is regular whereas in the former the weaker beat always follows the short interval. Pulsus paradoxus - the pulse volume normally decreases during inspiration, but this decrease is exaggerated when there is a reduced left ventricular stroke volume (cardiac tamponade, constrictive pericarditis), and transmission of negative intrathoracic pressure to the aorta (severe bronchial asthma, emphysema). Thus, the application of the term pulsus paradoxus, to a greater than normal decline in systolic arterial pressure (10 mm Hg or more) during inspiration, is wrong but it has the advantage of common and long usage. Although both the pulsus alternans and paradoxus can be appreciated at the radial pulse, they are easily recognized on sphygmomanometry. Tension. An estimation of tension (systolic pressure within the artery) can be obtained by compressing the brachial artery gradually until the radial pulse disappears. The force required to obliterate the brachial arterial pulse can be given by a figure which should approximate to the measured systolic pressure. The difference between the two gets smaller with experience. Other pulses must be examined now if the cardiovascular system alone is being examined, but the task can be deferred till the examination of the nervous system when it is convenient to feel for the pulses as well as test the tendon reflexes in the legs. You should decide upon a routine and stick to it. The other radial artery should be palpated simultaneously to compare the volume and tension in both radials. The femoral artery should be located in the inguinal region and felt to both sides, and if its volume is suspected to be low then it should be felt simultaneously with the radial to look for the radiofemoral delay. In obstructive lesions

47 of the aorta (coarctation of the aorta; atheroma, dissection, compression by a tumour) the femoral pulse, which is normally ahead of the radial, is delayed and reduced in volume. Of the other pulses the popliteal can be difficult to feel, particularly when it is important (namely in peripheral vascular insufficiency) to decide whether it is palpable and of normal volume. With the knee joint semiflexed the popliteal fossa should be palpated with both hands. In difficult cases the palpable pulse may be felt in the prone position. The posterior tibial and the dorsalis pedis pulses are comparatively easier to feel in their appropriate places. The carotid pulse because of its proximity to the heart can be very informative and, as an extension of the outflow tract, reflects faithfully the events at and below the aortic valve. It can be felt inside the sterno-mastoid muscle with the thumb. The anacrotic pulse can be appreciated by the pulp and the collapsing pulse can be felt as well by following movements of the thumb (Corrigan's sign). The waveform of the carotid pulse may be difficult to appreciate in some patients with a large adipose or muscular bulk. For this reason it is important to cultivate the habit of palpating the brachial pulse. Popov-Saveliev's sign (Saveliev N.A., Russian therapist; Popov V.O. - Russian physician) - a weakening of the pulse wave in the left radial artery, especially when lying on the left side (a sign of stenosis of the left atrioventricular opening).

Blood pressure This important task should be undertaken towards the end of the examination, or at least after 15 minutes rest, when the patient is more likely to be relaxed and accustomed to the environment and examination. Blood pressure is measured with a stethoscope and a sphygmomanometer. The width of the cuff should be about 40% of the circumference of the limb used for determining the blood pressure. The standard size, a 14 cm wide cuff, is used for adult with an arm of average size. The cuff width should be 7 cm for young children, and 22 cm for obese and heavily built subjects. The mercury manometer should be kept at a level corresponding to the heart of the patient to rule out the influence of gravity. 48

The cuff should be wrapped firmly around the upper arm and air pumped while the brachial or radial pulse is felt. As the pressure in the cuff exceeds the systolic pressure within the brachial artery the pulse becomes impalpable. This pressure should be noted and the cuff deflated. Next the bell of the stethoscope should be placed lightly over the brachial artery in the antecubital fossa and the above procedure repeated. After the pressure has reached the previously noted level, the cuff should be deflated gradually. The passage of blood past the decreasing obstruction creates a series of sounds (named after Korotkoff, a naval surgeon who first described them) which are audible through the stethoscope. The first loud sound (phase I) approximates to systolic pressure. As the pressure in the cuff is further lowered, the sounds first become softer (phase II), then louder (phase III), as the volume of blood flow through the constricted artery increases. The sounds become muffled (phase IV) when the arterial caliber increases and the arterial diastolic pressure approaches. The point of disappearance of the Korotkoff sounds (phase V) is used to define diastolic pressure. It is a good practice to record the pressure both at phase IV and phase V. In aortic regurgitation and pregnancy the disappearance point may be very low when phase IV is much closer to the diastolic pressure. The systolic pressure should always be measured first by palpation, since in some patients with very high blood pressure the Korotkoff sounds may disappear then reappear again as the cuff pressure is lowered. This phenomena is called the auscultatory silent gap. The blood pressure should be measured in both arms if the pulse is weaker on one side, or if you suspect vertebrobasilar insufficiency with subclavian steal. In patients with orthostatic hypotension, the measurements should be taken both in the supine and the erect positions. In patients suspected of having coarctation or atheromatous disease of the aorta, blood pressure should be measured in the arm and in the thigh where the arterial systolic pressure, which is usually about 20 mm Hg higher than in the arm, may be lower. The cuff should be applied to the thigh in the prone position, and auscultation should be carried out over the popliteal fossa.

In pulsus alternans, the systolic pressure may vary by more than 10 mm Hg in alternate beats. This discrepancy can be recognized by alteration in the intensity of the Korotkoff sounds. In pulsus paradoxus, the peak systolic pressure during expiration may be higher by 10 mm Hg or more than the corresponding pressure during the entire cycle of respiration. Hill's sign (Hill L., 1866-1952, English physiologist, Nobel Prize winner in Physiology). Hill's sign is an increase of existing and normal difference of systolic blood pressure on the arms and legs. The normal systolic blood pressure on the legs (as measured by Korotkoff method) is higher than on the arms, but not more than 10-15 mm Hg. This is due to feebly marked augmentation (amplification) phenomenon, i.e. summing of the amplitudes of the incoming and reflected waves (forming the so-called «standing wave») in the lower limbs due to greater distance from the heart to the lower extremities in comparison with the upper limbs. It should be noted that during direct intravascular measurement, blood pressure on the legs is not higher than on the arms. Hill's sign occurs in hyperkinetic conditions due to even more enhancement (further augmentation) of blood wave at high stroke volume, when the value of «standing waves» (the «tsunami» 1 effect) can be significantly increased. This occurs in case of severe aortic insufficiency, hyperthyroidism and other hyperkinetic states.

CIRCULATORY FAILURE Circulatory failure is an extremely common problem with an incidence of 2% at age 50 years, rising to 10% at age 80 years. There is still a high mortality: 10—30% per year. Circulatory failure occurs when an adequate blood flow to the tissues cannot be maintained. This maybe caused by inadequate cardiac output (heart failure) or by a markedly reduced intravascular volume, for example after major haemorrhage, acute dehydration or in septicaemic shock (vascular failure). Heart failure (congestive heart failure) : Symptomatic myocardial dysfunction resulting in a characteristic pattern of hemodynamic, renal, and neurohormonal responses. 50

No definition of heart failure (HF) is entirely satisfactory. Congestive heart failure ( CHF ) develops when plasma volume increases and fluid accumulates in the lungs, abdominal organs (especially the liver), and peripheral tissues. Physiology At rest and during exercise, cardiac output (CO), venous return, and distribution of blood flow with O 2 delivery to the tissues are balanced by neurohumoral and intrinsic cardiac factors. Preload, the contractile state, afterload, the rate of contraction, substrate availability, and the extent of myocardial damage determine left ventricular (LV) performance and myocardial O 2 requirements. The Frank-Starling principle, cardiac reserve, and the oxyhemoglobin dissociation curve play a role. Preload (the degree of end-diastolic fiber stretch) reflects the end-diastolic volume, which is influenced by diastolic pressure and the composition of the myocardial wall. For clinical purposes, the end-diastolic pressure, especially if above normal, is a reasonable measure of preload in many conditions. LV dilatation, hypertrophy, and changes in myocardial distensibility or compliance modify preload. The contractile state in isolated cardiac muscle is characterized by the force and velocity of contraction, which are difficult to measure in the intact heart. Clinically, the contractile state is often expressed as the ejection fraction (LV stroke volume/end- diastolic volume). Afterload (the force resisting myocardial fiber shortening after stimulation from the relaxed state) is determined by the chamber pressure, volume, and wall thickness at the time of aortic valve opening. Clinically, afterload approximates systemic BP at or shortly after aortic valve opening and represents peak systolic wall stress. The heart rate and rhythm also influence cardiac performance. Reduced substrate availability (eg, of fatty acid or glucose), particularly if O2 availability is reduced, can impair the vigour of cardiac contraction and myocardial performance. Tissue damage (acute with myocardial infarction or chronic with fibrosis due to various diseases) impairs local myocardial performance and imposes an additional load on viable myocardium.

The Frank-Starling principle states that the degree of end-diastolic fiber stretch (preload) within a physiologic range is proportional to the systolic performance of the subsequent ventricular contraction This mechanism operates in HF, but, because ventricular function is abnormal, the response is inadequate. If the Frank-Starling curve is depressed, fluid retention, vasoconstriction, and a cascade of neurohumoral responses lead to the syndrome of CHF. Over time, LV remodeling (change from the normal ovoid shape) with dilatation and hypertrophy further compromises cardiac performance, especially during physical stress. Dilatation and hypertrophy may be accompanied by increased diastolic stiffness. Classification and Etiology In many forms of heart disease, the clinical manifestations of HF may reflect impairment of the left or right ventricle. Left ventricular (LV) failure characteristically develops in coronary artery disease, hypertension, and most forms of cardiomyopathy and with congenital defects (eg, ventricular septal defect, patent ductus arteriosus with large shunts). Right ventricular (RV) failure is most commonly caused by prior LV failure (which increases pulmonary venous pressure and leads to pulmonary arterial hypertension) and tricuspid regurgitation. Causes are also mitral stenosis, primary pulmonary hypertension, multiple pulmonary emboli, pulmonary artery or valve stenosis, and RV infarction. One distinguishes chrionic and acute heart failure. In Russian Federation clinicians use classification of chronic heart failure, stipulated by National Scientific Society of Cardiologists in 2002. It joins two classifications: one – after N.D. Strazhesko and V.H.Vasilenko (1935) and New York Heart Association functional classification (NYHA) (1964). According to this classification stages and functional classes of chronic heart failure are distinguished (Table 1 &6). Table 6 Stages of chronic heart failure (may worsen despite on treatment) I stage Initial stage of heart disease (damage). Hemodynamics

isn't altered. Latent heart failure. Asymtomatic left ventricular dysfunction. IIA stage Clinically pronounced stage of heart disease (damage). Hemodynamics is altered in one of circulation circles, moderately pronounced. Adaptive remodeling of the heart and vessels. IIB stage Grave stage of heart disease (damage). Pronounced hemodynamics alterations in both circulation circle. Disadaptive remodeling of the heart and vessels. III stage Terminal stage of the heart damage. Pronounced hemodynamics alterations and severe (irreversible) structural changes of target organs (heart, lungs, vessels, brain, kidneys). Final stage of organs remodeling.

HF is manifested by systolic or diastolic dysfunction or both. Combined systolic and diastolic abnormalities are common. In systolic dysfunction (primarily a problem of ventricular contractile dysfunction), the heart fails to provide tissues with adequate circulatory output. A wide variety of defects in energy utilization, energy supply, electrophysiologic functions, and contractile element interaction occur, which appear to reflect abnormalities in intracellular Ca++ modulation and cyclic adenosine monophosphate (cAMP) production. Systolic dysfunction has numerous causes; the most common are coronary artery disease, hypertension, and dilated congestive cardiomyopathy. There are many known and probably many unidentified causes for dilated myocardiopathy. More than 20 viruses have been identified as causal. Toxic substances damaging the heart include alcohol, a variety of organic solvents, certain chemotherapeutic drugs (eg, doxorubicin), β-blockers, Ca blockers, and antiarrhythmic drugs. Diastolic dysfunction (resistance to ventricular filling not readily measurable at the bedside) accounts for 20 to 40% of cases of HF. It is generally associated with prolonged ventricular relaxation time, as measured during isovolumic relaxation (the time between 53 aortic valve closure and mitral valve opening when ventricular pressure falls rapidly). Resistance to filling (ventricular stiffness) directly relates to ventricular diastolic pressure; this resistance increases with age, probably reflecting myocyte loss and increased interstitial collagen deposition. Diastolic dysfunction is presumed to be dominant in hypertrophic cardiomyopathy, circumstances with marked ventricular hypertrophy (eg, hypertension, advanced aortic stenosis), and amyloid infiltration of the myocardium. Pathophysiology In LV failure, CO declines and pulmonary venous pressure increases. Elevated pulmonary capillary pressure to the levels that exceed the oncotic pressure of the plasma proteins (about 24 mm Hg) leads to increased lung water, reduced pulmonary compliance, and a rise in the O 2 cost of the work of breathing. Pulmonary venous hypertension and edema resulting from LV failure significantly alter pulmonary mechanics and, thereby, ventilation/perfusion relationships. Dyspnea correlates with elevated pulmonary venous pressure and the resultant increased work of breathing, although the precise cause is debatable. When pulmonary venous hydrostatic pressure exceeds plasma protein oncotic pressure, fluid extravasates into the capillaries, the interstitial space, and the alveoli. Pleural effusions characteristically accumulate in the right hemithorax and later bilaterally. Lymphatic drainage is greatly enhanced but cannot overcome the increase in lung water. Unoxygenated pulmonary arterial blood is shunted past nonaerated alveoli, decreasing mixed pulmonary capillary PaO2. A combination of alveolar hyperventilation due to increased lung stiffness and reduced PaO2 is characteristic of LV failure. Thus, arterial blood gas analysis reveals an increased pH and a reduced PaO 2 (respiratory alkalosis) with decreased saturation reflecting increased intrapulmonary shunting.

Typically, PaCO 2 is reduced too. A PaCO 2 above normal signifies alveolar hypoventilation possibly due to respiratory muscle failure and requires urgent ventilatory support. In RV failure, systemic venous congestive symptoms develop. Moderate hepatic dysfunction commonly occurs in CHF secondary to RV failure, with usually moderate increases in conjugated and unconjugated bilirubin, prothrombin time, and hepatic enzymes (eg, alkaline phosphatase, AST, ALT). However, in severely compromised 54 circulatory states with markedly reduced splanchnic blood flow and hypotension, increases due to central necrosis around the hepatic veins may be severe enough to suggest hepatitis with acute liver failure. Reduced aldosterone breakdown by the impaired liver further contributes to fluid retention. In systolic dysfunction, inadequate ventricular emptying leads to increased preload, diastolic volume, and pressure. Sudden (as in MI) and progressive (as in dilated cardiomyopathy) myocyte loss induces ventricular remodeling, resulting in increased wall stress accompanied by apoptosis (accelerated myocardial cell death) and inappropriate ventricular hypertrophy. Later, the ejection fraction falls, resulting in progressive pump failure. Systolic HF may primarily affect the LV or the RV (see above), although failure of one ventricle tends to lead to failure of the other. In diastolic dysfunction, increased resistance to LV filling as a consequence of reduced ventricular compliance (increased stiffness) results in prolonged ventricular relaxation (an active state following contraction) and alters the pattern of ventricular filling. Ejection fraction may be normal or increased. Normally, about 80% of the stroke volume enters the ventricle passively in early diastole, reflected in a large e wave and smaller a wave on pulsed-wave Doppler echocardiography. Generally, in diastolic LV dysfunction the pattern is reversed, accompanied by increased ventricular filling pressure and a-wave amplitude. Whether the failure is primarily systolic or diastolic and regardless of which ventricle is affected, various hemodynamic, renal, and neurohumoral responses may occur. Hemodynamic responses : With reduced CO, tissue O2 delivery is maintained by increasing A-VO2. Measurement of A-VO2 with systemic arterial and pulmonary artery blood samples is a sensitive index of cardiac performance and reflects, via the Fick equation (VO2 = CO . A-VO2), CO (inversely related) and the body's O2 consumption (VO2--directly related). Increased heart rate and myocardial contractility, arteriolar constriction in selected vascular beds, venoconstriction, and Na and water retention compensate in the early stages for reduced ventricular performance. Adverse effects of these compensatory efforts 55 include increased cardiac work, reduced coronary perfusion, increased cardiac preload and afterload, fluid retention resulting in congestion, myocyte loss, increased K excretion, and cardiac arrhythmia. Renal responses : The mechanism by which an asymptomatic patient with cardiac dysfunction develops overt CHF is unknown, but it begins with renal retention of Na and water, secondary to decreased renal perfusion. Thus, as cardiac function deteriorates, renal blood flow decreases in proportion to the reduced CO, the GFR falls, and blood flow within the kidney is redistributed. The filtration fraction and filtered Na decrease, but tubular resorption increases. Neurohumoral responses : Increased activity of the renin-angiotensin-aldosterone system influences renal and peripheral vascular response in HF. The intense sympathetic activation accompanying HF stimulates the release of renin from the juxtaglomerular apparatus near the descending loop of Henle in the kidney. Probably, decreased arterial systolic stretch secondary to declining ventricular function also stimulates renin secretion. Reflex and adrenergic stimulation of the renin-angiotensin-aldosterone system produces a cascade of potentially deleterious effects: Increased aldosterone levels enhance Na reabsorption in the distal nephron, contributing to fluid retention. Renin produced by the kidney interacts with angiotensinogen, producing angiotensin I from which is cleaved the octapeptide angiotensin II by ACE. Angiotensin II has various effects believed to enhance the syndrome of CHF, including stimulation of the release of arginine vasopressin (AVP), which is antidiuretic hormone (ADH); vasoconstriction; enhanced aldosterone output; efferent renal vasoconstriction; renal Na retention; and increased norepinephrine release. Angiotensin II is also believed to be involved in vascular and myocardial hypertrophy, thus contributing to the remodeling of the heart and peripheral vasculature, which contributes to HF in various myocardial and other heart diseases. Plasma norepinephrine levels are markedly increased, largely reflecting intense sympathetic nerve stimulation, because plasma epinephrine levels are not increased. High plasma norepinephrine levels in patients with CHF are associated with a poor prognosis. The heart contains many neurohormonal receptors ( α1, β1, β2, β3, adrenergic, muscarinic, endothelin, serotonin, adenosine, angiotensin II). In patients with HF, β1 56 receptors (which constitute 70% of cardiac β receptors), but not the other adrenergic receptors, are down-regulated, potentially adversely affecting myocardial function. This down-regulation, which is probably a response to intense sympathetic overdrive, has been detected even in asymptomatic patients with the early stages of HF. Altered myocardial stimulator or receptor functions for various other neurohormonal factors may adversely influence myocyte performance in HF. Serum levels of atrial natriuretic peptide (released in response to increased atrial volume and pressure load) and brain natriuretic peptide (released from the ventricle in response to ventricular stretch) are markedly increased in patients with CHF. These peptides enhance renal excretion of Na, but, in patients with CHF, the effect is blunted by decreased renal perfusion pressure, receptor down-regulation, and perhaps enhanced enzymatic degradation. Serum, brain (B-type) natriuretic peptide appears to be important for diagnosis in CHF and correlates well with functional impairment. AVP is released in response to a fall in BP or ECF volume and by the effects of various neurohormonal stimuli. An increase in plasma AVP diminishes excretion of free water by the kidney and may contribute to the hyponatremia of HF. AVP levels in CHF vary, but experimental AVP blockers have increased water excretion and serum Na levels. Other consequences : Protein-losing enteropathy characterized by marked hypoalbuminemia, ischemic bowel infarction, acute and chronic GI hemorrhage, and malabsorption may result from severe chronic venous hypertension. Peripheral gangrene in the absence of large vessel occlusion or chronic irritability and decreased mental performance may result from chronic markedly reduced PO2, reflecting severely reduced cerebral blood flow and hypoxemia. Cardiac cachexia (loss of lean tissue >= 10%) may accompany severely symptomatic HF. The failing heart produces tumor necrosis factor-, which is a key cytokine in the development of catabolism and possibly of cardiac cachexia. Marked anorexia is characteristic of this syndrome. Restoring cardiac function to normal can reverse cardiac cachexia. Symptoms and Signs

HF may be predominantly right-sided or left-sided and may develop gradually or suddenly (as with acute pulmonary edema). Cyanosis may occur with any form of HF. The cause may be central and may reflect hypoxemia. A peripheral component due to capillary stasis with increased A-VO2 and resultant marked venous oxyhemoglobin unsaturation may also be present. Improved color of the nail bed with vigorous massage suggests peripheral cyanosis. Central cyanosis cannot be altered by increasing local blood flow. LV failure : Pulmonary venous hypertension may become apparent with tachycardia , fatigue on exertion , dyspnea on mild exercise, and intolerance to cold. Paroxysmal nocturnal dyspnea and nocturnal cough reflect the redistribution of excess fluid into the lung with the recumbent position. Occasionally, pulmonary venous hypertension and increased pulmonary fluid manifest as bronchospasm and wheezing. Cough may be prominent, and pink-tinged or brownish sputum due to blood and the presence of HF cells is common. Frank hemoptysis due to ruptured pulmonary varices with massive blood loss is uncommon but may occur. Signs of chronic LV failure include diffuse and laterally displaced apical impulse, palpable and audible ventricular (S3) and atrial gallops (S4), accentuated pulmonic second sound, and inspiratory basilar rales (crepitation). Right- sided pleural effusion is common. Acute pulmonary edema is a life-threatening manifestation of acute LV failure secondary to sudden onset of pulmonary venous hypertension. A sudden rise in LV filling pressure results in rapid movement of plasma fluid through pulmonary capillaries into the interstitial spaces and alveoli. The patient presents with extreme dyspnea, deep cyanosis, tachypnea, hyperpnea, restlessness, and anxiety with a sense of suffocation. Pallor and diaphoresis are common. The pulse may be thready ( pulsus filiformis ), and BP may be difficult to obtain. Respirations are labored, and moist bubbling rales are widely dispersed over both lung fields anteriorly and posteriorly. Some patients manifest marked bronchospasm or wheezing (cardiac asthma). Noisy respiratory efforts often render cardiac auscultation difficult, but a summation gallop, merger of S3 and S4, may be heard. Hypoxemia is severe. CO2 retention is a late, ominous manifestation of secondary hypoventilation and requires immediate attention. 58

RV failure: The principal symptoms include fatigue; awareness of fullness in the neck; fullness in the abdomen, with occasional tenderness in the right upper quadrant (over the liver); ankle swelling; and, in advanced stages, abdominal swelling due to ascites. Edema over the sacrum is likely in supine patients. Signs include evidence of systemic venous hypertension, abnormally large a or v waves in the external jugular pulse, an enlarged and tender liver, a murmur of tricuspid regurgitation along the left sternal border, RV S3 and S4, and pitting edema of the lowest parts of the body Diagnosis Although symptoms and signs (eg, exertional dyspnea, orthopnea, edema, tachycardia, pulmonary rales, a third heart sound, jugular venous distention) have a diagnostic specificity of 70 to 90%, the sensitivity and predictive accuracy are low. Elevated levels of B-type natriuretic peptide are diagnostic. Adjunctive tests include CBC, blood creatinine, electrolytes (eg, Mg, Ca), glucose, albumin, and liver function tests. Thyroid function test results should be assessed in patients with atrial fibrillation and in selected, especially older, persons. In patients with suspected coronary artery disease, stress testing with radionuclide or ultrasound imaging or coronary angiography may be indicated. Endocardial biopsy is of limited usefulness. ECG should be performed in all patients with HF, although findings are not specific; ambulatory ECG is not generally useful. Various abnormalities (eg, of ventricular hypertrophy, MI, or bundle branch block) may provide etiologic clues. Recent onset of rapid atrial fibrillation may precipitate acute LV or RV failure. Frequent premature ventricular contractions may be secondary and may subside when the HF is treated. Chest x-ray should be performed in all patients (Fig.25 &26). Pulmonary venous congestion and interstitial or alveolar edema are characteristics of pulmonary edema. Kerley B lines reflect chronic elevation of left atrial pressure and chronic thickening of the intralobular septa from edema.

Fig.25. Heart failure The upper zone blood vessels are distended and there are linear densities in the periphery of the lower zones (in terstitial or Kerley‘s B lines) and there are some areas of apparent consolidation, indicating alveolar pulmonary edema.

Fig.26 Heart failure following myocardial infarction.

Microvascular volume increases, most strikingly in dependent areas, ie, the bases in upright posture. Careful examination of the cardiac silhouette, evaluation of chamber enlargement, and a search for cardiac calcifications may reveal important etiologic clues. Echocardiography can help evaluate chamber dimensions, valve function, ejection fraction, wall motion abnormalities, and LV hypertrophy. Doppler or color Doppler echocardiography accurately detects pericardial effusion, intracardiac thrombi, and tumors and recognizes calcifications within the cardiac valves, mitral annulus, and the wall of the aorta. Underlying coronary artery disease is strongly suggested by localized or segmental wall motion abnormalities. Doppler studies of mitral and pulmonary venous inflow are often useful in identifying and quantitating LV diastolic dysfunction. Other important investigations include a full blood count to in order to exclude anaemia, urea and electrolytes, thyroid function tests, liver function tests and cardiac enzymes if recent infarction is suspected. Vascular failure. Circulatory failure of vascular origin occurs in disorder of normal ratio between vascular bed capacity and circulating blood volume. It develops in blood volume decrease (blood loss, dehydration), or in vascular tonus drop. The latter frequently depends on: 1) reflex disturbance of vascular vasomotor innervation in traumas, serous tunic irritation, myocardial infarction, pulmonary artery embolism etc; 2) vascular vasomotor innervation disturbance of cerebral origin (in hypercapnia, acute hypoxia of oliencephalon, psychogenic reactions); З) vascular paresis of toxic origin, which is observed in plural infections and intoxications. Vascular tonus drop leads to disorder of body blood distribution: deposited blood volume increases, particularly in vessels of abdominal viscera, and circulating blood volume decreases. Circulating blood volume decrease involves decrease of the heart venous return, decrease of stroke volume, decrease of arterial and venous pressures. Vascular circulatory failure may be acute and in this case is called collapse . Circulating blood volume decrease and arterial pressure fall leads to cerebral ischemia, hence such symptoms as dizziness (vertigo), blackout, ringing in patient‘s ears are characteristic for 61 acute vascular failure; loss of consciousness is frequently observed. On physical examination pallor, diaphoresis, extremity coldness, quick hypopnoe, weak, sometimes thready pulse, blood pressure fall are noticed. Syncope refers to acute vascular failure manifestations, it is transitory loss of consciousness due to insufficient cerebral blood supply. Syncope may appear in over fatigue, frightened condition, stuffy rooms. It is caused by central nervous regulation disorder of vascular tonus, leading to blood accumulation in abdominal vessels. In syncope pallor, diaphoresis, extremity coldness, weak or thready pulse are noticed. In some people inclination to syncope is observed in change of supine position to vertical, especially in young asthenics, more frequently in women. Over fatigue, anemia, carried-out infectious disease are predisposing factors. Such syncope is called orthostatic collapse . It is explained by insufficiently fast reaction of vasomotor apparatus, owing to that in patient‘s position change the blood rushes from upper body half into lower extremities and abdominal cavity vessels. HYPERTENSION Arterial hypertension is elevation of systolic (systolic BP >= 140 mm Hg) and/or diastolic BP (>= 90 mm Hg,), either primary or secondary, which can damage the walls of arteries, arterioles and the left ventricle of the heart with serious consequences, chiefly affecting the brain, heart, kidneys and eyes. Prevalence It is one of the most common disorders in the Western world, with a prevalence of about 15%. It is estimated that there are nearly 50 million hypertensives in the USA and about 27 % of all patients with cardiovascular disease in Russia. Hypertension occurs more often in black adults (32%) than in white (23%) adults, and morbidity and mortality are greater in blacks. Diastolic BP increases with age until age 55 or 60. Prevalence of isolated systolic hypertension (ISH-- >= 140 mm Hg systolic, < 90 mm Hg diastolic) increases with age until at least age 80. If persons with ISH and diastolic hypertension are considered, > 50% of black and white men and > 60% of women over age 65 have hypertension. ISH is more prevalent among women than men in 62 both races. Between 85 and 90% of cases are primary (essential); in 5 or 10%, hypertension is secondary to bilateral renal parenchymal disease or endocrinopathy , and only 1 or 2% of cases are due to a potentially curable condition. Etiology and Pathogenesis Primary hypertension : Primary (essential) hypertension is of unknown etiology; its diverse hemodynamic and pathophysiologic derangements are unlikely to result from a single cause. The term ―hypertensive disease is used in Russia. Heredity is a predisposing factor, as shown by the relevance of a family history of hypertension and by racial variations in prevalence. but the exact mechanism is unclear. Environmental factors (eg, dietary Na, obesity, stress) seem to act only in genetically susceptible persons. The pathogenic mechanisms must lead to increased total peripheral vascular resistance (TPR) by inducing vasoconstriction, to increased cardiac output (CO), or to both because BP equals CO (flow) times resistance. Although expansion of intravascular and extravascular fluid volume is widely claimed to be important, such expansion can only raise BP by increasing CO (by increasing venous return to the heart), by increasing TPR (by causing vasoconstriction), or by both; it frequently does neither. Abnormal Na transport across the cell wall due to a defect in or inhibition of the Na-K pump (Na+,K+-ATPase) or due to increased permeability to Na+ has been described in some cases of hypertension. The net result is increased intracellular Na, which makes the cell more sensitive to sympathetic stimulation. Because Ca follows Na, it is postulated that the accumulation of intracellular Ca (and not Na per se) is responsible for the increased sensitivity. Na+,K+-ATPase may also be responsible for pumping norepinephrine back into the sympathetic neurons to inactivate this neurotransmitter. Thus, inhibition of this mechanism could conceivably enhance the effect of norepinephrine. Defects in Na transport have been described in normotensive children of hypertensive parents. Stimulation of the sympathetic nervous system raises BP, usually more in hypertensive or prehypertensive patients than in normotensive patients. Whether this hyperresponsiveness resides in the sympathetic nervous system itself or in the 63 myocardium and vascular smooth muscle that it innervates is unknown, but it can often be detected before sustained hypertension develops. A high resting pulse rate, which can be a manifestation of increased sympathetic nervous activity, is a well-known predictor of subsequent hypertension. Some hypertensive patients have a higher-than-normal circulating plasma catecholamine level at rest, especially early in clinical development. In the renin-angiotensin-aldosterone system , the juxtaglomerular apparatus helps regulate volume and pressure. Renin, a proteolytic enzyme formed in the granules of the juxtaglomerular apparatus cells, catalyzes conversion of the protein angiotensinogen to angiotensin I. This inactive product is cleaved by a converting enzyme, mainly in the lung but also in the kidney and brain, to angiotensin II, which is a potent vasoconstrictor that also stimulates release of aldosterone. Also found in the circulation, the angiotensin III is as active as angiotensin II in stimulating aldosterone release but has much less pressor activity. Renin secretion is controlled by at least four mechanisms that are not mutually exclusive: A renal vascular receptor responds to changes in tension in the afferent arteriolar wall; a macula densa receptor detects changes in the delivery rate or concentration of NaCl in the distal tubule; circulating angiotensin has a negative feedback effect on renin secretion; and the sympathetic nervous system stimulates renin secretion via the renal nerve mediated by receptors. The mosaic theory states that multiple factors sustain elevated BP even though an aberration of only one was initially responsible; eg, the interaction between the sympathetic nervous system and the renin-angiotensin-aldosterone system. Sympathetic innervation of the juxtaglomerular apparatus in the kidney releases renin; angiotensin stimulates autonomic centers in the brain to increase sympathetic discharge. Angiotensin also stimulates production of aldosterone, which leads to Na retention; excessive intracellular Na enhances the reactivity of vascular smooth muscle to sympathetic stimulation. Hypertension leads to more hypertension. Other mechanisms become involved when hypertension due to an identifiable cause (eg, catecholamine release from a pheochromocytoma, renin and angiotensin from renal artery stenosis, aldosterone from an 64 adrenal cortical adenoma) has existed for some time. Smooth muscle cell hypertrophy and hyperplasia in the arterioles resulting from prolonged hypertension reduce the caliber of the lumen, thus increasing TPR. In addition, trivial shortening of hypertrophied smooth muscle in the thickened wall of an arteriole will reduce the radius of an already narrowed lumen to a much greater extent than if the muscle and lumen were normal. This may be why the longer hypertension has existed, the less likely surgery for secondary causes will restore BP to normal. Deficiency of a vasodilator substance rather than excess of a vasoconstrictor (eg, angiotensin, norepinephrine) may cause hypertension. The kallikrein system, which produces the potent vasodilator bradykinin, is beginning to be studied. Extracts of renal medulla contain vasodilators, including a neutral lipid and a prostaglandin; absence of these vasodilators due to renal parenchymal disease or bilateral nephrectomy would permit BP to rise. Modest hypertension sensitive to Na and water balance is characteristic for anephric persons (renoprival hypertension). Endothelial cells produce potent vasodilators (nitric oxide, prostacyclin) and the most potent vasoconstrictor, endothelin. Therefore, dysfunction of the endothelium could have a profound effect on BP. The endothelium's role in hypertension is being investigated. Evidence that hypertensive persons have decreased activity of nitric oxide is preliminary. Secondary hypertension: Secondary hypertension is associated with renal parenchymal disease (eg, chronic glomerulonephritis or pyelonephritis, polycystic renal disease, collagen disease of the kidney, obstructive uropathy) or pheochromocytoma, Cushing's syndrome , primary aldosteronism , hyperthyroidism, myxedema, coarctation of the aorta, or renovascular disease . It may also be associated with the use of excessive alcohol, oral contraceptives, sympathomimetics, corticosteroids, cocaine, or licorice. Hypertension associated with chronic renal parenchymal disease results from combination of a renin-dependent mechanism and a volume-dependent mechanism. In most cases, increased renin activity cannot be demonstrated in peripheral blood, and careful attention to fluid balance usually controls BP. 65

Pathologic anatomy. No early pathologic changes occur in primary hypertension. Large and medium-sized arteries respond to high blood pressure by thickening of the media and disruption of the elastic tissue within their walls. The vessels may become tortuous and dilated and may rupture because of the high pressure in the lumen. If this occurs in the brain, cerebral haemorrhage usually leaves the patient dead or paralysed from a stroke. Hypertension also promotes the formation of atheroma in medium-sized and large arteries, so a stroke may also be caused by occlusion of a cerebral artery by thrombus formed on an atheromatous plaque, or by embolization of atheromatous material from plaques in the extracranial segments of the carotid arteries or aorta. Atheroma formation in the coronary arteries renders hypertensive patients susceptible to angina pectoris, myocardial infarction and sudden death. In smaller arteries and arterioles, hypertension causes prominent thickening of the intima, in addition to medial hypertrophy. In cases of “accelerated” or “malignant” hypertension, in which the blood pressure is very high or has risen quickly, these intimal changes can occlude the vessels, producing distal tissue ischemia. This particularly affects the kidneys, causing renal failure. The walls of the small arteries in the brain may be damaged so that their permeability is increased and cerebral edema results, causing hypertensive encephalopathy characterized by headache, confusion, fits and coma. There may also be visual disturbances due to retinal arterial damage, which may be seen on examination of the fundi. The left ventricle responds to high blood pressure by hypertrophy. Initially, this increases its force of contraction and maintains a normal cardiac output, but eventually the hypertrophied muscle outgrows its oxygen supply and angina and cardiac failure result. Ultimately, generalized arteriolar sclerosis develops; it is particularly apparent in the kidney (nephrosclerosis) and is characterized by medial hypertrophy and hyalinization. Nephrosclerosis is the hallmark of primary hypertension.

Damage of target organs. Hypertension, particularly long-term existing, leads to viscera damage, called target organs, - heart, vessels, brain and kidneys. The heart damage in hypertension may declare itself by left ventricular hypertrophy and affecting of coronary vessels with angina pectoris, myocardial infarction development, and also sudden cardiac death. In heart damage progressing the heart failure develops. Myocardial ischemia may appear not only due to coronary arteries affection (their epicardiac parts), but due to relative coronary insufficiency (unchanged coronary arteries inability to supply with blood hypertrophied myocardium), and due to microvasculopathy. Vessels damage. Vessels, directly participating in high BP maintenance due to TPR, are themselves one of target organs. Vascular damage is characterized by involving in process retinal vessels, carotids, aorta (aneurysms), and also affecting of small vessels: damage of cerebral vessels (occlusions or microaneurysms) may lead to stroke, renal arteries – to renal functions alteration. Fundi investigation allows physician to assess directly vessels changes. In hypertension vessels narrow, then expose to sclerosis, that is accompanied by microaneurysms and microhemorrhages formation, and also by ischemic damage of blood supplying organs. All these changes may be stage by stage observed on patient's fundus of eye. Brain damage is characterized by thrombosis and hemorrhages, hypertensive encephalopathy and lacunae formation in brain tissues. Cerebral vessels damage may lead to changes of their walls (atherosclerosis). In various stages of disease these changes may be complicated by stroke due to thrombosis or cerebral vessels rupture with hemorrhage. Kidneys damage . As early as initial stage of disease there is inclination to renal vessels changes, at first, with some increase, and then decrease of glomerular filtration. Long-term course of hypertension leads to nephroangiosclerosis with significant impairment of renal functions and chronic renal failure development. Renal functions reflect changes of glomerular filtration rate (GFR). If on initial stage of hypertension GFR is usually normal, on later stages (or in malignant hypertension) it 67 progressively decreases. Furthermore, creatinine blood level and protein urine concentration (microalbuminuria is typical) are the indicators of kidneys involvement in pathologic process. Hemodynamics Not all patients with primary hypertension have normal CO (cardial output) and increased TPR. CO is increased, and TPR is inappropriately normal for the level of CO in the early labile phase of primary hypertension. TPR increases and CO later returns to normal, probably because of autoregulation. Patients with high, fixed diastolic pressures often have decreased CO. The role of the large veins in the pathophysiology of primary hypertension has largely been ignored, but venoconstriction early in the disease may contribute to the increased CO. Plasma volume tends to decrease as BP increases, although some patients have expanded plasma volumes. Hemodynamic, plasma volume, and PRA variations are evidence that primary hypertension is more than a single entity or that different mechanisms are involved in different stages of the disorder. Renal blood flow gradually decreases as the diastolic BP increases and arteriolar sclerosis begins. GFR remains normal until late in the disease, and, as a result, the filtration fraction is increased. Coronary, cerebral, and muscle blood flow are maintained unless concomitant severe atherosclerosis is present in these vascular beds. In the absence of heart failure, CO is normal or increased, and peripheral resistance is usually high in hypertension due to pheochromocytoma, primary aldosteronism, renal artery disease, and renal parenchymal disease. Plasma volume tends to be high in hypertension due to primary aldosteronism or renal parenchymal disease and may be subnormal in pheochromocytoma. Systolic hypertension (with normal diastolic pressure) is not a discrete entity. It often results from increased CO or stroke volume (eg, labile phase of primary hypertension, thyrotoxicosis, arteriovenous fistula, aortic regurgitation); in elderly persons with normal or low CO, it usually reflects inelasticity of the aorta and its major branches (arteriosclerotic hypertension).

Hypertension and risk of cardiovascular complications. Risk factors . Prognosis in patients with hypertension depends not only on BP level. Important meaning have risk factors, divided on main (basic) and additional (Table 7). Table 7

Main (basic) risk factors Additional risk factors

1. men and menopause women 1. reduced HDL cholesterol level 2. smoking 2. raised LDL cholesterol level 3. cholesterol >6,5mmol/L 3. diabetes mellitus 4. family history of premature 4. impaired glucose tolerance cardiovascular disease 5. obesity (women<65y., men - <55 y) 6. sedentary life-style 7. raised fibrinogen 8. endogenous tissular plasminogen activator 9. inhibitor of plasminogen activator type I 10. hyperhomocysteinemia 11. D- dimmer 12. raised C-reactive protein 13. oestrogens deficiency 14. Chlamydia pneumoniae 15. social-economic state 16. ethnicity

On risk evaluation main factors are usually used, among additional factors - cholesterol fractions, obesity, impaired glucose tolerance - are chosen. Stratification of patients by absolute level of cardiovascular risk Decisions about the management of patients with hypertension should not be based on the level of blood pressure alone, but also on the presence of other risk factors, concomitant diseases such as diabetes, target organ damage, and cardiovascular or renal disease, as well as other aspects of the patient's personal, medical and social situation (Table 8). Four categories of absolute cardiovascular disease risk are defined (low, medium, high and very high risk) (Table 9). Each category represents a range of absolute disease

69 risks. Within each range, the risk of any one individual will be determined by the severity and number of risk factors present. So, for example, individuals with very high levels of cholesterol or a family history of premature cardiovascular disease in several first-degree relatives will typically have absolute risk levels that are at the higher end of the range provided. Similarly, individuals with other risk factors listed in Table 8 may also have absolute risk levels that are towards the higher end of the range for the category. How well these estimates predict the absolute risk of cardiovascular disease in Asian, African or other non-Western populations is uncertain. In those countries CHD incidence is relatively low and heart failure or renal disease is more common. Table 8. Factors Influencing Prognosis (according to WHO guidelines,1999). Risk Factors For Target Organ Damage1 Associated Clinical Cardiovascular Diseases Conditions2 I. Used for risk -Left ventricular Cerebrovascular disease stratification hypertrophy -ischaemic stroke -Levels of systolic and (electrocardiogram, -cerebral haemorrhage diastolic blood pressure echocardiogram or -transient ischaemic attack (Grades 1-3) radiogram) Heart disease -Men >55 years -Proteinuria and/or slight -myocardial infarction -Women >65 years elevation of plasma -angina -Smoking creatinine concentration (1. -coronary revascularisation -Total cholesterol >6.5 2 - 2.0 mg/dl) -congestive heart failure mmo/l (250 mg/dl) -Ultrasound or radiological Renal disease -Diabetes evidence of atherosclerotic -diabetic nephropathy -Family history of plaque (carotid, iliac and -renal failure (plasma premature cardiovascular femoral arteries, aorta) creatinine concentration >2.0 disease -Generalised or focal mg/dl) II. Other factors adversely narrowing of the retinal Vascular disease influencing prognosis arteries -dissecting aneurysm

-Reduced HDL -symptomatic arterial disease cholesterol Advanced hypertensive -Raised LDL cholesterol retinopathy -Microalbuminuria in -haemorrhages or exudates diabetes -papilloedema -Impaired glucose tolerance -Obesity -Sedentary lifestyle -Raised fibrinogen -High risk socioeconomic group -High risk ethnic group -High risk geographic region

1 - "Target Organ Damage" corresponds to previous WHO Stage 2 hypertension 2 "Associated Clinical Conditions" corresponds to previous WHO Stage 3 hypertension. Table 9. Stratification of Risk to Quantify Prognosis Other Risk Grade 1 Grade 2 Grade 3 Factors & SBP 140-159 or SBP 160-179 or SBP і 180 or Disease History DBP 90-99 DBP 100-109 DBP і 110 I. no other risk LOW RISK MED RISK HIGH RISK factors II. 1-2 risk MED RISK MED RISK V HIGH RISK factors III. 3 or more risk HIGH RISK HIGH RISK V HIGH RISK

71 factors or TOD1 or diabetes IV. ACC2 V HIGH V HIGH V HIGH RISK RISK RISK Risk strata (typical 10 year risk of stroke or myocardial infarction): Low risk = less than 15%; medium risk = about 15-20% risk; high risk = about 20-30%; very high risk = 30% or more 1. TOD – Target Organ Damage (Table 2) 2. ACC – Associated Clinical Conditions, including clinical cardiovascular disease or renal disease (Table 8) Classification of essential hypertension (hypertensive disease) According to great attention to cardiovascular risk evaluation in hypertensive patients there is designed transition to classifications with distinction of BP elevation grades with simultaneous risk assessment (low, medium, high, very high). This approach was stipulated in WHO and ISAH experts recommendations (1999) and was supported in Russian national recommendations on AH (2000). Recently used in Russia classifications are presented below. Until now classification of essential hypertension (hypertensive disease) by WHO (1962) is widespread in Russia. Classification of essential hypertension (hypertensive disease) by WHO (1962). I stage — BP elevation >160/95 mmHg without organic changes of cardiovascular system; II stage — BP elevation > 160/95 mmHg in combination with changes of target organs (heart, kidneys, brain, fundal vessels), caused by hypertension, but without their functional alterations; III stage — hypertension, combined with target organs damage (heart, kidneys, brain, fundal vessels) with their functional alterations.

Table 10 Definitions and Classification of Blood Pressure Levels

Recently both classifications are recommended in Russia; it is necessary to indicate stage of disease as well as BP grade. Clinical manifestations depend on damage of target organs. Many of patients are asymptomatic, and frequently hypertension is detected occasionally. There may be neurosis signs, headaches, particularly in the mornings; nausea, flashing of ―midges in front of eyes; pain in precordium, palpitation, rapid fatigability, epistaxis (nasal bleedings), hyperexcitability, irritability, sleep disturbance. In later stages coronary events may appear. Severity of these symptoms, in particular, headaches, not always corresponds to BP elevation grade. On medical history analysis it is necessary to obtain information about family history of hypertension as well as other conditions, worsening prognosis in their presence – diabetes mellitus, coronary heart disease, stroke, dyslipidemia. Information about duration and level of BP arising, previous drug and non-pharmaceutical therapy effectiveness are important. It is necessary to elicit patient's lifestyle peculiarities, including diet (fats, excessive salt and alcohol consumption), smoking, physical activity level, excessive body mass or obesity. On examination one attracts attention on excessive body mass. A face hyperemia as well as pallor due to peripheral arteriolar spasm are noticed. On heart examination sign of left ventricular hypertrophy (apical impulse shift to the left) - key syndrome in hypertension - is detected, that confirmed by ECG, X-ray and,

73 especially, ECO examinations. On elevated BP there is typical pulse strain increase, due to grade of which may be approximately assessed level of BP. Moreover, elevated BP is characterized by accent of S2 at the aorta appearance. ECG changes are initially characterized by decrease of T-wave amplitude in the left chest leads. Left ventricular hypertrophy is revealed by high-amplitude R-wave with oblique depression of ST segment in V4-6. Left bundle-branch block may develop. On ECO hypertrophy of interventricular septum and left ventricular posterior wall is verified. Sometimes these changes are accompanied by dilatation, increase of end-systolic and end-diastolic left ventricular dimensions. Appearance of hypokinetic and even dyskinetic zones in the myocardium is the sign of left ventricular contractile capacity decline. Different metabolic disorders: hyperinsulinemia, impaired glucose tolerance (in some cases – diabetes mellitus, type II), dyslipidemia (reduced HDL cholesterol, raised LDL cholesterol), obesity were frequently marked during last years. Hypertensive crisis . Clinical course of hypertension may be complicated by hypertensive crisis. It is fast, additional, significant BP rise. It may be provoked by different physical and mental loading, excessive dietary sodium, water, alcohol intake; cessation of drug therapy. Very high BP is detected in patient (diastolic BP may exceed 130—140 mmHg). In the majority of cases on the background of such BP elevation cerebral signs (nausea, vomiting, vision reduction) appear. Simultaneously or later other signs and complications of hypertension may increase: coronary heart disease (CHD) exacerbation, acute left-sided heart failure occurrence and stroke. On severe crisis fundal hemorrhages, papilledema may appear. Kidneys damage. During the late stage of hypertension due to arteriolosclerosis development the signs of kidneys damage appear: impaired concentrative capacity, decrease of urine relative density, proteinuria, hematuria, and in the terminal stage – azotic wastes retention. Parallel signs of eyes fundum damage develop: increasing retinal arteries narrowing and tortuosity, especially in comparison with veins; veins dilation, may be fundal hemorrhages, and later degenerate foci in retina.

Central nervous system damage determines various signs, concerned with intensity and location of vascular disorders. Vascular narrowing (due to their spasm) leads to focal brain ischemia with partial fall-out of its functions and in more severe cases is accompanied by brain hemorrhages. In sharp BP elevation there may be arterial wall ruptures with massive hemorrhage. Primary hypertension is asymptomatic until complications in target organs develop (eg, left ventricular failure, atherosclerotic heart disease, cerebrovascular insufficiency with or without stroke, renal failure). Dizziness, flushed facies, headache, fatigue, epistaxis, and nervousness are not caused by uncomplicated hypertension. A fourth heart sound and broad, notched P-wave abnormalities on the ECG are among the earliest signs of hypertensive heart disease. Echocardiographic evidence of left ventricular hypertrophy may appear later. Chest x-ray is often normal until the late dilated phase of hypertensive heart disease. Aortic dissection or leaking aneurysm of the aorta may be the first sign of hypertension or may complicate untreated hypertension. Polyuria, nocturia, diminished renal concentrating ability, proteinuria, microhematuria, cylindruria, and nitrogen retention are late manifestations of arteriolar nephrosclerosis. Retinal changes may include retinal hemorrhages, exudates, papilledema, and vascular accidents. On the basis of retinal changes, Keith, Wagener, and Barker classified hypertension into groups that have important prognostic implications: group 1-- constriction of retinal arterioles only; group 2--constriction and sclerosis of retinal arterioles; group 3--hemorrhages and exudates in addition to vascular changes; group 4 (malignant hypertension)--papilledema. Diagnosis Diagnosis of primary hypertension depends on repeatedly demonstrating higher- than-normal systolic and/or diastolic BP and excluding secondary causes

ATHEROSCLEROSIS. ISCHEMIC HEART DISEASE Atherosclerosis is a form of arteriosclerosis characterized by patchy subintimal thickening (atheromas) of medium and large arteries, which can reduce or obstruct blood flow. Atherosclerotic plaque consists of accumulated intracellular and extracellular lipids, 75 smooth muscle cells, connective tissue, and glycosaminoglycans. Circulating low-density lipoprotein (LDL) migrate through the endothelial barrier of the arterial wall and penetrate into the intima. Some plaques, covered by a thin fibrous cap, may undergo spontaneous fissure or rupture. These plaques are unstable or vulnerable and are more closely associated to the onset of an acute ischemic event. Ischemic heart disease (IHD; also known as coronary heart disease (CHD) is usually caused by structural disorder of the coronary arteries (coronary artery disease − CAD). Ischemic heart disease produces six clinical syndromes: - angina pectoris − stable or unstable, and variant; - myocardial infarction (MI); - postMI cardiosclerosis or old MI; - heart failure; - arrhythmias; - sudden cardiac death.

Ischemic heart disease has uncontrollable (advanced age, male sex, genetic predisposition) and modifiable [smoking (risk is almost double), hypertension (risk is double if systolic blood pressure is >180 mm Hg), hyperlipidemia, glucose intolerance or diabetes mellitus, obesity (weight >30% over ideal), hypothyroidism, left ventricular hypertrophy (LVH), sedentary life-style, oral contraceptive use, cocaine use, low serum folates level) risk factors. Angina pectoris is characterized by discomfort that occurs when myocardial oxygen demand exceeds the supply. Myocardial ischemia can be asymptomatic (silent ischemia), particularly in diabetics. Pain is located behind the sternum. The usual distribution is referral to all or part of the sternal region, the left side of the chest, and the neck and down the ulnar side of the left forearm and hand. The most important diagnostic factor is the history. The physical examination is of little diagnostic help and may be totally normal in many patients. An ECG taken during the acute episode may show transient T-wave inversion or ST- segment depression or elevation (may be either convex and concave), but some patients may have a normal tracing.

Fig.27. ECG before, during attack of angina pectoris and after taking nitrates.

Ambulatory (Holter) electrocardiographic monitoring can detect silent ischemia (ischemic ECG changes without accompanying symp-toms), which occur in >50% of patients with unstable angina. Coronary angiography is performed to define the location and extent of coronary disease; this is indicated in selected patients who are candidates for CABG (coronary artery bypass grafting) surgery or angioplasty. Myocardial infarction (MI) is characterized by necrosis resulting from an insufficient supply of oxygenated blood to an area of the heart. One distinguishes: - non−Q wave MI: Area of ischemic necrosis is limited to the inner one third to half of myocardial wall; - Q wave MI: Area of ischemic necrosis penetrates the entire thickness of the ventricular wall. MI may be caused by • Coronary atherosclerosis • Coronary artery spasm • Coronary embolism (caused by infective endocarditis, rheumatic heart disease, intracavitary thrombus) • Periarteritis and other coronary artery inflammatory diseases • Dissection into coronary arteries (aneurysmal or iatrogenic) • Congenital abnormalities of coronary circulation • MI with normal coronaries (MINC syndrome): more frequent in younger patients and cocaine addicts. Echocardiography can evaluate wall motion abnormalities and identify mural thrombus or mitral regurgitation, which can occur acutely after MI. Clinical presentation of MI: • Crushing substernal or retrosternal chest pain usually lasts longer than 30 min. • Pain is unrelieved by rest or sublingual nitroglycerin or is rapidly recurring. • Pain radiates to the left or right arm, neck, jaw, back, shoulders, or abdomen and is not pleuritic in character. • Pain may be associated with dyspnea, diaphoresis, nausea, or vomiting. 78

• There is no pain in approximately 20% of infarctions (usually in diabetic or elderly patients). Physical findings: Skin may be diaphoretic, with pallor (because of decreased oxygen). • Rales may be present at the bases of lungs (indicative of CHF). • Cardiac auscultation may reveal an apical systolic murmur caused by mitral regurgitation secondary to papillary muscle dysfunction; S3 or S4 may also be present. • Physical examination may be completely normal. • Serum cardiac enzyme studies: damaged necrotic heart muscle releases cardiac isoenzymes (CK, LDH) into the blood stream in amounts that correlate with the size of the infarct. Electrophoretic fractionation of the enzymes can pinpoint certain isoenzymes (CK-MB and LDH-1) that are more sensitive indicators of MI than total CK or LDH. • Cardiac troponin levels: cardiac-specific troponin T (cTnT) and cardiac- specific troponin I (cTnI) are new markers for acute Ml. On the ECG in Q wave infarction, there is development of: Common signs 1. (-)T: (ischemia); 2. ST ABOVE CONTOUR, a synonym for "monophasic curve" (damage heart muscle); 3. PATHOLOGICAL Q (necrosis of the heart muscle): the extension Q > 0,03; Q > 1/4R; 4. The DISCORDANCE of the OFFSET ST: ST in leads opposite to the localization of infarction; 5. DYNAMICS (acute phase (injury)-acute-subacute-cicatricial stage). STAGE OF MIOCARDICAL INFARCTION (table 11). 1. Stage of ISCHEMIA; 2. PREACUTE phase (stage of injury): ST above contour; 3. In the ACUTE stage (formation of necrosis): ST above contour with the transition in (-) T; the formation of pathological Q;

4. SUBACUTE stage (resorption, proliferation, reparation and organization in the scar area): ST on the contour, T (-), pathological Q; 5. SCAR stage (final consolidation of the scar): ST on the contour, T (-) or (+), pathological Q – in this case, the sign of the scar.

The duration of the stages is subject to the rule of the Troika and the increases on the rise: (ISCHEMIA PHASE), up to 3 days (PREACUTE STAGE), to 3 weeks (ACUTE PHASE), to 3 months (SUBACUTE STAGE), the rest of life (SCAR STAGE). Table 11. STAGE OF MIOCARDICAL INFARCTION STAGE DURATION SIGN Stage of high pointed (coronary) T ISCHEMIA to 30 min wave

PREACUTE ST above contour phase up to 3 days

ACUTE stage to 3 weeks ST above contour with the transition in (-) T; the

formation of pathological Q; SUBACUTE ST on the contour, T (-), stage to 3 months pathological Q;

SCAR stage the rest of life ST on the contour, T (-) or (final (+), pathological Q consolidation of the scar)

LOCALIZATION OF IM (Fig. 28-29): 1. The FRONT wall of the left ventricle: I, aVL, V1-4; discordant displacement to ST III, aVF; 2. The SIDE wall of the left ventricle: V5-6; 3THE LOWER wall LV: III, aVF; the discordance of the offset ST in I, aVL

Fig.28. MI of the front wall of the left ventricle.

Fig.29. MI of the lower wall of the left ventricle. 81

TEST CONTROL: 1. THE PATIENT COMPLAINS OF PROLONGED (MORE THAN 10 MIN.) CHEST PAIN OF INCREASING CHARACTER, RADIATING TO THE BACK, ARM AND NECK, RESULTING IN A STATE OF REST AND NOT STOPED AFTER TAKING 3 TABLETS OF NITROGLYCERIN. WHAT KIND OF PATHOLOGY YOU CAN THINK OF (GIVE ONE ANSWER)? a) cardialgia; b) angina; c) angina at rest; d) myocardial infarction; e) pericarditis; f) dissecting aneurysm of the aorta.

2. INDICATE THE 5 CHARACTERISTIC SYMPTOMS OF RIGHT HEART FAILURE: a) enlargement of the liver; b) shortness of breath during physical exertion and/or at rest; c) attacks of breathlessness with difficulty in inhalation and exhalation, forcing to take a half upright position; d) attacks of breathlessness with difficulty exhaling, forcing to take a sitting position with fixation of the shoulder girdle; e) presence of free fluid in the abdomen (ascites); f) the presence of free fluid in the pleural cavity (hydrothorax); g) the presence of free fluid in the pericardial cavity (hydroperiod); h) swelling of the feet.

3. PERCUSSION BORDERS OF RELATIVE CARDIAC DULLNESS OF THE PATIENT REVEALED THE FOLLOWING DATA: - right margin – 1 cm outwards from the right edge of the sternum, - left – 4 cm laterally from the left midclavicular line, - upper – in intercostal space III, - the width of the vascular bundle – 5 cm. For what configuration of the heart is typical? a) for normal; b) for the mitral; c) for aortic.

4. WHAT ARE 2 FACTORS MOST DETERMINE THE LEVEL OF DIASTOLIC BLOOD PRESSURE (BP)? a) the tone of resistive vessels (arterioles) – total peripheral vascular resistance; b) the volume of the vascular of ejection (stroke volume of the heart); c) the elasticity of the walls of the aorta; d) the completeness of closure of the valves of the aorta.

5. DURING THE INSPECTION AND PALPATION OF THE HEART REGION OF THE PATIENT REVEALED AMPLIFIED AND DIFFUSE APEX BEAT. WHAT STATE OF HEART IS THE EVIDENCE? a) only hypertrophy of the left ventricle; b) only dilatation of the left ventricle; c) only dilatation of the right ventricle d) hypertrophy of the left ventricle and dilatation of the left ventricle

6. LIST THE FEATURES CHARACTERIZING HEART DISEASES EDEMA: a) a high density edema ("solid" edema); b) low density edema (soft swelling); c) pallor of the skin in the area of edema; d) cyanotic skin in the area of edema; e) the presence of trophic skin changes in the area of edema; f) lack of trophic skin changes in the area of edema.

7. EXPLAIN THE MECHANISM OF OCCURRENCE OF COUGH WITH CLEAR SPUTUM AND HEMOPTYSIS IN PATIENTS WITH LEFT VENTRICULAR HEART FAILURE (GIVE ONE ANSWER): a) inflammatory process in the alveoli – the exudation of blood plasma and red blood cells; b) high pressure in the blood vessels of the pulmonary circulation – the leakage of blood plasma and erythrocytes in the alveoli; c) high pressure in the blood vessels of the big circle of blood circulation – the leakage of blood plasma and erythrocytes in the alveoli; d) high pressure in the blood vessels of the pulmonary circulation – bronchial vessels microreserve – penetration of blood plasma into the lumen of the bronchi. 8. WHAT ARE 3 METHODS OF PHYSICAL AND INSTRUMENTAL EXAMINATION CAN REVEAL DILATATION OF THE LEFT VENTRICLE? a) palpation of the heart;

83 b) percussion of the heart; c) electrocardiography (ECG); d) roentgenography of chest organs; e) echocardiography (EchoCG).

9. HOW TO CHANGE THE LOCALIZATION OF THE APEX BEAT OF THE WOMAN IN THE LAST 2-3 MONTHS OF PREGNANCY? a) will not change; b) shift up and to the left; c) will shift to the right.

10. PALPATION OF THE PATIENT IN THE APEX OF THE HEART REVEALED A THRILL THAT DOES NOT COINCIDE WITH THE PULSATION OF THE APEX BEAT. FOR WHAT CONDITION IS THIS TYPICAL? a) obstruction of blood flow through the mitral valve hole; b) obstruction of blood flow through the opening of the tricuspid valve; c) obstruction of blood flow through the opening of the aortic valve. 11. SPECIFY 3 MAIN COMPONENTS INVOLVED IN THE FORMATION OF I TONE OF THE HEART: a) fluctuations of the valves of the atrioventricular valves in the phase of isometric reduction; b) fluctuations of the valves of the valves of the aorta and pulmonary artery protodiastolic period; c) fluctuations in the muscular wall of the ventricles in the phase of isometric contraction; d) fluctuations in the muscular wall of the ventricle at protodiastolic period; e) oscillations of initial segments of the aorta and pulmonary artery in the early phase of exile.

12. SPECIFY THE MAIN 4 MECHANISM OF WEAKENING OF THE II TONE IN THE SECOND INTERCOSTAL SPACE RIGHT OF STERNUM: a) increase the mobility of the semilunar valves of the aorta; b) reducing the mobility of the semilunar valves of the aorta; c) non-tight closing of the valves of the aorta in the protodiastolic period; d) lowering the pressure in the aorta; e) the increase in the rate of relaxation of ventricular myocardium; f) decrease in the rate of relaxation of the ventricular myocardium.

13. WHAT ARE 3 OF THE LISTED SIGNS CAN BE USED TO IDENTIFY THE I HEART TONE? a) the tone coincides with the apex beat and carotid pulsation; b) a tone does not coincide with the apex beat and carotid pulsation; c) the tone is listened after a long pause; d) the tone is listened after a short pause; e) a low frequency tone and long lasting.

14. HOW TO CHANGE THE VOLUME OF I TONE AT THE APEX IN MITRAL VALVE INSUFFICIENCE? a) increase; b) decrease; in) will not change.

15. WHAT 2 CHANGES II TONE OF THE HEART CAN REVEAL IN THE 2ND INTERCOSTAL SPACE LEFT OF STERNUM IN PATIENTS PRESENTING COMPLAINTS OF SIGNIFICANT DYSPNEA AND A COUGH WITH STREAKS OF BLOOD, INCREASING IN A HORIZONTAL POSITION AND DECREASING IN ORTHOPNEA POSITION? a) gain (emphasis) II tone; b) weakining II tone; c) no change II tone.

16. SPECIFY THE 2 CHARACTERISTIC AUSCULTATION SIGNS OF ATRIAL FIBRILLATION: a) correct (regular) rhythm of the heart; b) isolated premature occurring I and II heart tones followed by a pause on the background of the right rhythm; c) completely irregular (chaotic) rhythm of the heart; d) the same volume I of tones in each cardiac cycle; e) the constant change of volume I of the tone ( from one cardiac cycle to another). 17. WHEN REGISTERING PHONOCARDIOGRAM (FKG) AT THE APEX OF THE HEART, THE PATIENT RECORDED HIGH-FREQUENCY DIASTOLIC EXTRATONE ARISING FROM CLOSE II TONE (EVERY 0.1 S). NAME IT: a) III the tone of the heart; b) IV is the heart; c) the tone of the opening of the mitral valve.

18. 2 SPECIFY THE SYMPTOMS OF THE PHYSIOLOGICAL SPLITTING OF II HEART SOUND: a) the constancy of this phenomenon; b) the impermanence of this phenomenon; c) the appearance during inhalation.

19. THE PATIENT HAS A PRONOUNCED ATHEROSCLEROTIC DISEASE OF THE ASCENDING AORTA AND AORTIC VALVE. MYOCARDIAL CONTRACTILITY OF THE LEFT VENTRICLE SATISFACTORY, THE AMPLITUDE OF THE DISCLOSURE OF THE AORTIC VALVE IS SUFFICIENT. WHAT IS THE LIKELY CHANGE IN II TONE IN THE SECOND INTERCOSTAL SPACE TO THE RIGHT OF THE STERNUM? a) enhanced II tone (accent II tone on the aorta); b) weakened II tone; in) II unmodified tone. 20. THE PATIENT HAS LARGE FOCUS OF POSTINFARCTION CARDIOSCLEROSIS OF THE LEFT VENTRICLE AND OBJECTIVE SIGNS OF MYOGENIC DILATATION (THE WEAKENING AND SHIFT TO THE LEFT OF THE DIFFUSE APEX BEAT, OFFSET TO THE LEFT RELATIVE DULLNESS OF THE HEART). WHAT 3 CHANGES OF HEART TONES WE CAN IDENTIFY IN THIS SITUATION? a) the strengthening of tone I on the top; b) I weakening tone at the apex; c) increased the I tone at the base of the xiphoid process; d) the appearance of the pathological III tone heart at the apex; f) the appearance of the pathological IV tone heart at the apex; g) appearance at the top of the tone of mitral valve opening.

21. GIVE THE DEFINITION OF "VALVULAR REGURGITATION" (CHOOSE ONE ANSWER): a) any turbulent blood flow through the valve opening; b) turbulent blood flow through the sash of the diseased valve during systole; c) turbulent blood flow through the sash of the diseased valve in diastole; d) blood flow through the affected valve flaps, incapable of full closure; e) blood flow through the affected valve flaps, are not able to fully open.

22. SPECIFY THE NATURE AND AREA OF THE BEST LISTENING OF MURMURS, IF THE PATIENT HAS THE MITRAL STENOSIS: a) systolic murmur at the apex; b) diastolic murmur at the apex; c) systolic murmur in the second intercostal space to the right of the sternum; d) diastolic murmur in the second intercostal space to the right of the sternum; e) systolic murmur in the second intercostal space left of the sternum;

23. SPECIFY THE NATURE AND AREA OF THE BEST LISTENING OF MURMURS, IF THE PATIENT HAS PULMONARY ARTERY VALVE INSUFFICIENCE a) systolic murmur at the apex; b) diastolic murmur at the apex; c) systolic murmur in the second intercostal space to the right of the sternum; d) diastolic murmur in the second intercostal space to the right of the sternum; e) systolic murmur in the second intercostal space left of the sternum; f) diastolic murmur in the second intercostal space left of the sternum; g) systolic murmur at the base of the xiphoid process.

24. SPECIFY THE NATURE AND AREA OF THE BEST LISTENING OF MURMURS, IF THE PATIENT HAS SWELLING AND PULSATION OF THE JUGULAR VEINS OF THE NECK, COINCIDING WITH THE PULSATION OF THE APEX BEAT? a) systolic murmur at the apex; b) diastolic murmur at the apex; c) systolic murmur in the second intercostal space to the right of the sternum; d) diastolic murmur in the second intercostal space to the right of the sternum; e) systolic murmur in the second intercostal space left of the sternum; f) diastolic murmur in the second intercostal space left of the sternum; g) systolic murmur at the base of the xiphoid process.

25. WHAT 2 GROUPS OF HEART MURMURS ARE FUNCTIONAL? a) murmurs resulting from lesions of the heart valves and great vessels; b) murmur occurring due to a decrease in blood viscosity or increased blood flow velocity; c) murmur arising from the relative insufficiency or valve stenosis holes;

87 d) pericardial RUB and pleuropericardial murmur; e) the murmur arising from congenital heart defects. 26. ON SOME OF THESE HEART LESIONS CAN BE CONSIDER IF THE PATIENT STUDY REVEALED: INCREASED I TONE AND MESOCESTOIDES LOW FREQUENCY RUMBLING MURMUR AT THE APEX OCCURRING AFTER AN AUDIBLE TONE BY OPENING OF THE MITRAL VALVE? a) mitral valve insufficiency; b) mitral stenosis; c) the aortic insufficiency; d) aortic stenosis.

27. HOW TO CHANGE THE LOUDNESS OF THE SYSTOLIC MURMUR OF MITRAL REGURGITATION WITH INCREASING THE CONTRACTILITY OF THE LEFT VENTRICLE? a) decreases; b) will increase; in) will not change.

28. GIVE A DETAILED CHARACTERIZATION OF THE MURMUR ORGANIC MITRAL REGURGITATION (GIVE ANSWER 4): a) auscultated at the apex; b) is the systolic; c) is the diastolic; d) starts immediately after the I tones; e) starts some time after I tone; f) is held in the left axillary region; g) is carried out on the carotid and subclavian arteries.

29. GIVE A DETAILED CHARACTERIZATION OF THE ORGANIC MURMUR OF AORTIC VALVE INSUFFICIENCY (GIVE 5 ANSWERS): a) auscultated in the 2nd intercostal space right of the sternum; b) auscultated in the 2nd left intercostal space from the sternum; c) auscultated left of the sternum, in the area of attachment of III – IV ribs; d) is the systolic; e) is diastolic; f) starts immediately after the II tone;

88 g) starts some time after II tone; h) is held in the left axillary region; i) is carried out according to the flow of blood from the aorta into the left ventricle.

30. SPECIFY 2 PERCUS AND RADIOGRAPHIC SYMPTOM OF MITRAL CONFIGURATION OF THE HEART: a) displacement of right border of relative dullness of heart to the right; b) the offset of the left border of relative dullness of heart to the left; c) the displacement of the upper borders of relative dullness of the heart upward; d) accentuated waist of heart; e) waist smoothed heart.

31. DESCRIBE THE APEX BEAT IN A PATIENT WITH MITRAL VALVE INSUFFICIENCY IN THE STAGE OF COMPENSATION DEFECT (REPLY 3): a) enhanced apex beat; b) weakened apex beat; c) the displacement of the apex beat to the left only; d) the displacement of the apex beat to the left and down (6th – 7th intercostal space); e) apex beat advanced; f) apex beat concentric.

32. CHECK THE 4 TYPICAL SYMPTOMS OF DECOMPENSATION OF MITRAL HEART DEFECTS: a) acrocyanosis; b) dense bluish swelling of legs and feet; c) fluid effusion in the pleural cavity; d) shortness of breath on exertion; e) pain in the heart area character (removed nitroglycerin); f) enlargement of the liver.

33. HOW TO CHANGE THE PERCUS SHAPE OF THE HEART IN A PATIENT WITH MITRAL VALVE STENOSIS AT THE STAGE OF COMPENSATION (ONE ANSWER) a) displacement of the upper border of relative dullness of heart - up, and the waist smoothed heart. ; b) significant shift of the left border of relative dullness of heart to the left.

34. WHICH 3 OF THE FOLLOWING COMPLAINTS ARE CHARACTERISTIC FOR A MITRAL VALVE INSUFFICIENCY PATIENT? a) shortness of breath during physical exertion and in the supine position; b) pain in the heart area and behind the breastbone radiating to the left arm and under the shoulder blade; c) sensations of faults in work of heart and heartbeat ("chaotic rhythm hearts"); d) swelling of the feet (more towards evening); e) dizziness and (sometimes) momentary fainting during physical load; f) dyspnea and cough with blood streaks at night. 35. WHAT ARE 2 VARIATIONS OF THE PULSE AT THE RADIAL ARTERIES ARE TYPICAL OF PATIENTS WITH MITRAL VALVE STENOSIS WITH ATRIAL FIBRILLATION? a) high and imminent ("galloping" - pulse Corrigan); b) low and slow; c) pulsus deficience; d) different (pulsus difference); e) pulsus paradoxus.

36. SPECIFY 2 AUSCULTATION SIGN OF ATRIAL FIBRILLATION : a) correct the heart rhythm; b) single failures in the activities of the heart on the background of the right rhythm; c) "chaotic" (completely irregular) heart rhythm; d) strengthening of tone I at the apex; e) changing the volume I tone at the apex.

37. SPECIFY 3 MAIN DIAGNOSTIC AUSCULTATION SIGNS OF STENOSIS THE MITRAL VALVE (RHEUMATIC ETIOLOGY): a) the strengthening of tone I at the apex; b) I weakening tone at the apex; c) the presence of pathological III tone at the apex; d) the presence of the tone of mitral valve opening at the apex; e) low-frequency diastolic murmur at the apex without holding in other areas. 38. SPECIFY 2 PERCUSSION AND RADIOGRAPHIC CHARACTERISTIC AORTIC CONFIGURATION OF THE HEART:

90 a) displacement of right border of relative dullness of heart to the right; b) the offset of the left border of relative dullness of heart to the left; c) the displacement of the upper borders of relative dullness of the heart upward; d) accentuated waist of heart; e) waist smoothed heart.

39. DESCRIBE THE APEX BEAT IN A PATIENT WITH AORTIC VALVE INSUFFICIENCY IN THE STAGE OF COMPENSATION (3 ANSWERS): a) enhanced apex beat; b) weakened apex beat; c) displacement apex beat to the left; g) shifting apex beat to the left and down (the sixth to seventh intercostal space); d) no significant bias apex beat; e) apex beat diffuse.

40. HOW TO CHANGE THE PERCUS SHAPE OF THE HEART IN A PATIENT WITH AORTIC VALVE STENOSIS IN THE STAGE OF COMPENSATION (ONE ANSWER)? a) displacement of right border of relative dullness of heart to the right; b) significant shift of the left border of the heart to the left; c) the offset the upper border of the heart upward; d) the absence of significant displacements of the heart boundaries.

41. WHICH 3 OF THE FOLLOWING COMPLAINTS ARE CHARACTERISTIC IN FOR PATIENT SUFFERING FROM AORTIC VALVE INSUFFICIENCY (3ANSWERES)? a) dyspnea during physical exertion and in the supine position; b) pain in the heart area and behind the breastbone radiating to the left arm and under the shoulder blade; c) persistent sensations of faults in work of heart ("chaotic rhythm"); d) swelling of the feet (more towards evening); e) dizziness and (sometimes) momentary fainting during physical load; f) dyspnea and unproductive cough with streaks of blood at night; g) heartbeat, feeling of pulsation in the whole body.

42. DESCRIBE THE PULSE IN A PATIENT WITH AORTIC VALVE INSUFFICIENCY (GIVE ONE ANSWER).

91 a) high and imminent ("galloping" – pulse Corrigan); b) low and slow; c) scarce (pulsus deficience); d) different (pulsus difference).

43. SPECIFY 2 MAIN DIAGNOSTIC AUSCULTATION SIGNS OF THE AORTIC VALVE STENOSIS (RHEUMATIC ETIOLOGY): a) strengthening II tone of the aorta; b) the weakening of the II tone over the aorta; c) systolic murmur in the second intercostal space to the right of the sternum and at the point Botkin, performed in the vessels of the neck; d) systolic murmur at the apex

44. WHAT ARE 2 VALIDLY DISTINGUISH CHARACTERISTIC OF PAIN SYNDROME DEVELOPING IN A PATIENT WITH MYOCARDIAL INFARCTION FROM ANGINAL PAIN IN A PATIENT WITH ANGINA? a) localization of pain; b) nature of pain (pressure, burning, etc.); c) irradiation; d) the duration of the pain; e) the relationship of pain to physical load; f) the relationship of pain to the taking nitroglycerin; g) the relationship of pain to take validol.

45. WHICH 3 OF THE FOLLOWING SIGNS ARE THE MOST INFORMATIVE FOR RECOGNITION OF ACUTE MYOCARDIAL INFARCTION (MI)? a) a history of clinical manifestations of IHD (angina, myocardial infarction etc.); b) onset of the disease with prolonged chest pain, not stoped nitroglycerin; c) the beginning of disease with rise in temperature, cough and the appearance of intense sweep-ing pain in the left 1/2 of the thorax, worse on inspiration; d) increasing the left border of the relative dullness of the heart; e) the weakening of the heart sounds; f) fluctuations in blood pressure; g) appearance of ECG pathological Q wave (or QS complex) or of changes in ST segment or T wave; h) appearance of ECG signs of atrial fibrillation and increase of alkaline phosphatase activity in blood serum on the 2nd day of illness;

92 i) increasing the activity of aspartic (and/or alanine) transaminase in the blood serum on the 2nd day .

46. IN SOME CASES, THE Q-WAVE ON ECG IS CONSIDERED TO BE PATHOLOGICAL? a) its amplitude (depth) is greater than 1/4 of the amplitude of the tine's; b) its amplitude exceeds 1/4 of the amplitude of the R wave; c) its amplitude is less than 1/4 of the amplitude of the R wave; d) right (a) and (b); e) its duration is greater than 0, 04; f) its duration is 0.02 s.

47. WHAT ARE 3 LABORATORY AND INSTRUMENTAL TEST MAY BE USEFULL TO CONFIRM THE DIAGNOSIS OF ACUTE MYOCARDIAL? a) defining in the dynamics of leukocyte count and value of the erythrocyte sedimentation rate (a General blood test); b) determine the dynamics in the number of lymphocytes and platelets (General analysis of blood); c) the sample with physical exercise (Bicycle ergometry, the test for "treadmill"); d) echocardiography; e) phonocardiography; f) radionuclide study of the heart (myocardial scintigraphy).

48. HOW TO CHANGE THE VOLUME OF THE II HEART SOUND IN THE SECOND INTERCOSTAL SPACE TO THE RIGHT OF THE STERNUM IN A PATIENT WITH HYPERTENSION DISEASE? a) decreases; b) will increase; c) will not change.

49. WHAT IS THE CHANGE OF THE HEART CAN REVEAL IN A PATIENT WITH HYPERTENSION WHO HAS A LONG HISTORY (SINGLE ANSWER)? a) left ventricular hypertrophy; b) hypertrophy of the right ventricle; C) hypertrophy of both ventricles.

50. 3 SPECIFY THE CONDITION, THE RISK OF WHICH INCREASES SUBSTANTIALLY IN PATIENTS WITH HYPERTENSION: a) chronic inflammatory lung diseases; b) ischemic heart disease (angina, myocardial infarction); c) diabetes mellitus; d) rheumatism; e) acute violations of cerebral circulation (brain stroke); f) atherosclerosis of the aorta and its branches; g) myocarditis.

Application

Fig.1. Mitral incompetence

Fig.2. The position of the apical four -chamber hearts: a color Doppler study of the early diastolic filling of the left ventricle. Registers a unidirectional movement of blood in the pulmonary veins, left atrium and left ventricle towards the apex of the heart. L V — left

ventricle, LA — left atrium, RV — right ventricle, RA — right atrium, RSPV — right superior pulmonary vein.

Fig.3 The position of the apical four-chamber hearts. Color Doppler study systolic. Severe mitral insufficiency. The jet has a large diameter at the level of the cusps of the mitral valve, the flow reaches the opposite wall of the left atrium occupies almost all the left atrium and enters the pulmonary veins — these traits characterize severe mitral regurgitation.

Fig.4. Mitral stenosis

Fig.5.Aortic incompetence

Fig.6. Aortic regurgitation, the severity — from small to moderate. Color Doppler study of the position of the parasternal long axis of left ventricle. Motley regulatorului flow begins at the level of closing of the flaps of the aortic valve. LV — left ventricle, LA — left atrium, RV — right ventricle, Ao — ascending aorta, AR — aortic regurgitation.

Fig.7.Aortic stenosis

References: 1. Избранные вопросы пропедевтики внутренних болезней : издание для студентов и практикующих врачей . Часть 1/ В.А. Семенов , В.в. гноевых , Е.А. Черкашина , А.Ю. Смирнова ; под . Ред . Проф . В.В. Гноевых .- Ульяновск , 2014.- 208 с. 2. Internal diseases propedeutics / Ivashkin V.T., Okhlobystin A.V. - М. : ГЭОТАР - Медиа , 2014.- 176 с.; 3. Пропедевтика внутренних болезней . Учебно -методическое пособие . Часть VI. Introduction to internal diseases. Manual. Part VI. / Ослопов В.Н., Садыкова А.Р., Карамышева И.В. – Казань : КГМУ , 2006. - 75 с.

100