Internal diseases propedeutics. Part II. Diagnostics of …mail.ru/2017... · 2017-12-22 · 1 Federal budgetary educational establishment of higher education Ulyanovsk State University

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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

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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

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THE CONTENTS OF A TEXT BOOK

QUESTIONING OF PATIENTS WITH WITH CARDIOVASCULAR

DISEASES.

5

Main complains of patients with with cardiovascular diseases. 5

EXAMINATION OF PATIENTS WITH WITH CARDIOVASCULAR

DISEASES.

9

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

4

CIRCULATORY FAILURE 50

HYPERTENSION 62

ATHEROSCLEROSIS. ISCHEMIC HEART DISEASE 75

Angina pectoris 77

Myocardial infarction 78

TEST CONTROL 82

Application 95

References 99

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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

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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

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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

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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

filling

Pulmonary embolism, atrial myxoma

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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,

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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.

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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)

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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.

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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

pathological epigastric pulsation

Cardiac (right ventricular)

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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.

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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.

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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.

The level of diaphragm The right border of relative cardiac

dullness

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

dullness

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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.

The right border of relative cardiac dullness

absolute (total)

cardiac dullness

The left border of relative cardiac dullness

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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).

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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".

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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.

21

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

of the heart.

Fig.9. M

Aortic heart configuration

ostium and aortic incompetence

22

Radiography of the chest in combined heart defect shows mitral configuration

Fig.9. Mitral configuration II of the heart.

ortic heart configuration – the reasons of this configuration are

ortic incompetence, arterial hypertension.

shows mitral configuration

of the heart.

the reasons of this configuration are stenosis of aortic

23

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.


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

Aortic incompetence (insufficientia valvulae aortae

semilunar cusps close incompletely the aortic orifice and during diastole blood

regurgitates from aorta 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

causing its dilatation and taking

connective tissue expands on valvular cusps and deforms them. In sepsis ulcerous

endocarditis leads to destruction of valve parts, defects forming

subsequent scarring and shortening.


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

Radiography of the chest in aortic incompetence shows typical

configuration of the heart.

insufficientia valvulae aortae) is valve disease in which the


orta into left ventricle. Aortic regurgitation occurs if the aortic valve




sclerotic process at the base of valvular cusps leads to their wrinkling and

shortening. In syphilis and atherosclerosis pathologic process may

causing its dilatation and taking-up of valvular cusps without their affecting, or


endocarditis leads to destruction of valve parts, defects forming

subsequent scarring and shortening.




shows typical aortic

) is valve disease in which the


orta into left ventricle. Aortic regurgitation occurs if the aortic valve




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,

up of valvular cusps without their affecting, or


in the cusps and their



stretching on diastole. During systole left ventricle contracts with grater force t

aorta increased stroke volume. Left ventricle overwork leads to its hypertrophy, and

increase of systolic blood volume in aort

pressure within aorta during systole and diastole is characteris

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

"Trapezoidal" configuration of the heart

of the heart, angle between vena cava superior and right atrium and angle between right

atrium and diaphragm "disappear

(Fig.12).

Fig.12

" Spherical” configuration of the heart

the discharge of blood from the left to the right ventricle.

25

stretching on diastole. During systole left ventricle contracts with grater force t


increase of systolic blood volume in aorta causes its dilatation . Sharp fluctuation of blood

pressure within aorta during systole and diastole is characteristic for aortic incompetence.



ventricle during diastole, diastolic pressure rapidly decline (Application Fig.5

"Trapezoidal" configuration of the heart - the heart has a trapezoid shape, waist


atrium and diaphragm "disappear", the reason of configuration is hydropericardium

Fig.12 "Trapezoidal" configuration of the heart.

configuration of the heart when the ventricular septal defect

the discharge of blood from the left to the right ventricle.

stretching on diastole. During systole left ventricle contracts with grater force to eject into


. Sharp fluctuation of blood

tic for aortic incompetence.



(Application Fig.5-6).

the heart has a trapezoid shape, waist


configuration is hydropericardium

"Trapezoidal" configuration of the heart.

the ventricular septal defect due to

26

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.

"Cor bovinum" ("bull" heart)

hypertrophy and/or dilatation of its main offices in cardiomyopathy, advanced forms

heart failure.

27

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

Fig.15. "Cor bovinum"

the area of cardiac dullness is increased by

hypertrophy and/or dilatation of its main offices in cardiomyopathy, advanced forms of

28

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).

29

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

30

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 xifoideusattachment 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 point1. 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».

31

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:

32

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.

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

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. Such 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

time of the right ventricle and/or decrease of blood ejection time of the left ventricle

leads, respectively, to later appearance of pulmonary component and/or earlier appearance

of aortic component of S2 (Fig. 17

Fig. 17. Physiologic splitting of S

The pulmonic component of S

where S2 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

protodiastolic gallop rhythm

33


1. arterial pressure increase of various genesis (due to increase of aortic valve cusps



ch situation may appear, for example, in case of the right bundle

Doubling and splitting of S2 are, as a rule, associated with increase

time of the right ventricle and/or decrease of blood ejection time of the left ventricle


Fig. 17.).

Physiologic splitting of S2 can usually be detected in the 2

The pulmonic component of S2 is usually too faint to be heard at the apex or aortic area,

is single and derived from aortic valve closure alone.


increase of atrium volume may lead to appearance of pathologic third heart sound, or

protodiastolic gallop rhythm (Fig.18).


rease of aortic valve cusps



ch situation may appear, for example, in case of the right bundle

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


can usually be detected in the 2nd left interspace.

is usually too faint to be heard at the apex or aortic area,


pathologic third heart sound, or

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

lateral decubitus position. The bell of the stethoscope should be used with very light

pressure.

The fourth heart sound (S

in idiopathic hypertrophic subaortic stenosis. It has been attributed

distention associated with an augmented left atrial contraction and increased left

ventricular end-diastolic stretch (Fig. 19

very soft, low frequent and is found rather rarely, predomin

teenagers. Pathologic accentuation of S4 in adults is named as pre

Fig. 19. Fourth heart sound is an atrial contraction sound that occurs in late diastole,

preceding S1. S4 has a dull, low pitch, and heard

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

34

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


The fourth heart sound (S4) (presystolic) may be heard in systemic hy

pertrophic subaortic stenosis. It has been attributed


diastolic stretch (Fig. 19). In healthy people physiologic fourth sound is

very soft, low frequent and is found rather rarely, predomin

teenagers. Pathologic accentuation of S4 in adults is named as pre-systolic gallop rhythm.

Fourth heart sound is an atrial contraction sound that occurs in late diastole,

has a dull, low pitch, and heard better with the bell.



has been likened to a horse's gallop, and is called gallop of the third (Lup De

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


) (presystolic) may be heard in systemic hypertension and

pertrophic subaortic stenosis. It has been attributed to sudden ventricular


In healthy people physiologic fourth sound is

very soft, low frequent and is found rather rarely, predominantly in children and

systolic gallop rhythm.

Fourth heart sound is an atrial contraction sound that occurs in late diastole,

better with the bell.



the third (Lup De-da, Lup De-

35

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).

36

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

37

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

accentuation or prolonged

Slow rising pulse, low systolic pressure,

heaving apex beat, systolic thrill, ejection click,

Aortic stenosis

38

soft or absent A2

2. Ejection, as above. Loudest

in left 3rd, 4th interspace

Jerky pulse, atrial impulse over apex, lifting

apex beat

Hypertrophic obstructive

cardiomyopathy

3. Ejection, as above Hyperkinetic states, aortic incompetence,

complete heart block

Increased flow

4. Ejection, as above No signs Aortic stenosis

5. Ejection, over pulmonary

area

Increases during inspiration Pulmonary stenosis

6. Ejection, short, over

pulmonary area

Hyperkinetic states, left-to-right shunt (ASD,

VSD)

Increased flow

7. Late ejection, over mitral

area

Mid-systolic click Mitral valve prolapse

8. Pansystolic, blowing,

mostly uniform

Large volume pulse, displaced and vigorous

apex, right ventricular heave, S3, louder during

expiration

Mitral incompetence

9. Pansystolic, as above. Best

heard over left 3rd,

4th interspace

As above plus thrill frequently presents Ventricular septal defect

(VSD)

Table 4.

Chief diastolic murmurs

Time and quality Accompanying signs Interpretation

1. Early diastolic, high-

pitched, blowing

Collapsing pulse, Corrigan's sign, wide

pulse pressure, displaced and vigorous

apex

Aortic incompetence

2. Early diastolic, a short,

high-pitched whiff

Prominent 'a' wave, right ventricular heave,

loud P2

Graham Steell murmur

(functional pulmonary

incompetence)

3. Mid-diastolic, rough,

rumbling

Malar flush, small volume pulse, tapping

impulse, right ventricular heave, opening

snap

Mitral stenosis

4. Mid-diastolic, short, Signs of mitral incompetence, VSD or Inflow (mitral) murmur

following S3 patent ductus

5. Mid-diastolic, short,

over tricuspid area

Signs of atrial septal defect (ASD)

6. Continuous systolic and

diastolic, machinery noise

Collapsing pulse, thrill, mitral inflow

murmur

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 ventricle. 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

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. 22

Fig. 22. When the mitral valve fails to close fully in

left ventricle to left atrium, causing a murmur. S

the volume overload on the left ventricle.

39

patent ductus

Signs of atrial septal defect (ASD) Inflow (tricuspid) murmur

Collapsing pulse, thrill, mitral inflow

murmur

Patent ductus, aortopulmonary

septal defect



is characterized by diminished S1, systolic murmur appearance



icle. Minor degree of mitral incompetence isn't accompanied by S1


systolic murmur with maximal intensity at the apex (Application Fig.2

considerable intensity is registered at the left axilla. Systolic murmur is



has decrescent character. It may occupy all systole (pansystolic) or part of systole


2).

When the mitral valve fails to close fully in systole, blood regurgitates from

left ventricle to left atrium, causing a murmur. S1 is often decreased. An apical S

the volume overload on the left ventricle.

Inflow (tricuspid) murmur

Patent ductus, aortopulmonary

septal defect



is characterized by diminished S1, systolic murmur appearance



icle. Minor degree of mitral incompetence isn't accompanied by S1


(Application Fig.2). In severe valve

considerable intensity is registered at the left axilla. Systolic murmur is



has decrescent character. It may occupy all systole (pansystolic) or part of systole


systole, blood regurgitates from

is often decreased. An apical S3 reflects

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

typical of mitral stenosis melody called

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

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

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

lateral position will accentuate the murmur

Fig. 23. When the leaflets of the mitral valve thicken, stiffen, and become distorted,

the valve fails to open sufficiently in diastole. The

mid-diastolic (during rapid ventricular filling), and presystolic (during atrial contraction).

S1 is accentuated. An opening snap (OS) often follows S

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

40


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

is listened. Flapping S1, S2 and opening snap (OS) create the

typical of mitral stenosis melody called ―quail rhythm (Fig.23)


flow from the left atrium to the left ventricle on diastole (Application Fig.1



diastole beginning. However, murmur appears only at the end of diastole before the very

presystolic murmur, which appears in blood flow acceleration at the end of


may be preceded by an opening snap. Exercise and positioning the patient in the left

lateral position will accentuate the murmur (Fig.22).

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:

diastolic (during rapid ventricular filling), and presystolic (during atrial contraction).

is accentuated. An opening snap (OS) often follows S2 and initiates the murmur.


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


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 –

d opening snap (OS) create the

). A rumbling diastolic


Application Fig.1). This murmur



ears only at the end of diastole before the very

presystolic murmur, which appears in blood flow acceleration at the end of


p. Exercise and positioning the patient in the left

When the leaflets of the mitral valve thicken, stiffen, and become distorted,

resulting murmur has two components:

diastolic (during rapid ventricular filling), and presystolic (during atrial contraction).

and initiates the murmur.


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

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'

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

Fig. 24. Diastolic murmur in aortic regurgitation is located at the 2

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

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

murmur at the apex appears. Rarely diastolic (presystolic) 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

during active atrium systole. Sometimes in this valve disease two sounds (Traube's

doubling sound) and the Vinogradov

artery are revealed. They are explained by vibration of arterial wall on sy

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

systolic murmur, connected with blood flow across the narrow orifice, at the aorta is 41


lesion of aorta S2 may be clear enough.


Erb's point, which is best heard by sitting the patient upright,



Fig. 24).

Diastolic murmur in aortic regurgitation is located at the 2

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

patient sitting, leaning forward, with breath held in exhalation.


So, in large left ventricular dilatation relative mitral incompetence occurs and sy

murmur at the apex appears. Rarely diastolic (presystolic) murmur


diastole from aorta to left ventricle. It results in difficult blood flow f


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

on the heart auscultation at the apex diminished S1, connected with


diminished, in case of adhered valve cusps immobility it may not be heard. Rough

systolic murmur, connected with blood flow across the narrow orifice, at the aorta is



s point, which is best heard by sitting the patient upright,



Diastolic murmur in aortic regurgitation is located at the 2nd - 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


So, in large left ventricular dilatation relative mitral incompetence occurs and systolic

murmur at the apex appears. Rarely diastolic (presystolic) murmur - Flint's murmur


diastole from aorta to left ventricle. It results in difficult blood flow from LA to LV


Duroziez‘s doubling murmur heard over the femoral

artery are revealed. They are explained by vibration of arterial wall on systole and diastole

on the heart auscultation at the apex diminished S1, connected with


ve cusps immobility it may not be heard. Rough

systolic murmur, connected with blood flow across the narrow orifice, at the aorta is

characteristic. It radiates along blood flow direction to the carotids, and sometimes it may

be heard at the interscapular

Fig. 25. Midsystolic murmur in aortic stenosis is heard in the 2

space, radiates often to the neck and down the left sternal border, even to the apex. Heard

best with the patient sitting and leaning

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

for the clinical evaluation of the cardiovascular system.

Functional murmurs all 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

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

diseases.

Extracardiac murmurs

Pleuropericardial (pleural extrapericardial) rub

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

42


be heard at the interscapular area (Application Fig.7, Fig. 25).

Midsystolic murmur in aortic stenosis is heard in the 2


best with the patient sitting and leaning forward. A2 decreases as the stenosis worsens.


sessment, palpation of the abdomen for hepatomegaly, firm pressure

over the sacrum for dependent oedema, and auscultation over the lung bases are important

for the clinical evaluation of the cardiovascular system.

ll the functional murmurs are conditionally divided into three



neurosis, febrile conditions).

2. anemic murmurs, caused by decrease of blood viscosity and certain blood flow

acceleration in patients with anemias of different genesis;


caused by various valvular function lesions, including patients with organic card

Extracardiac murmurs

Pleuropericardial (pleural extrapericardial) rub occurs when the inflammation



synchronic with the heartbeats. To distinguish it from the true pericardial rub caused by


Midsystolic murmur in aortic stenosis is heard in the 2nd right intercostal


decreases as the stenosis worsens.


sessment, palpation of the abdomen for hepatomegaly, firm pressure

d auscultation over the lung bases are important

ll the functional murmurs are conditionally divided into three



ty and certain blood flow


caused by various valvular function lesions, including patients with organic cardiac

occurs when the inflammation



the true pericardial rub caused by

43

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

44

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.

45

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

46

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

47

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 thepulsus 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

48

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.

49

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.

50

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.

51

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 O2 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 O2 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.

52

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

53

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

54

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 O2 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 PaO2 (respiratory

alkalosis) with decreased saturation reflecting increased intrapulmonary shunting.

Typically, PaCO2 is reduced too. A PaCO2 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

55

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

56

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

57

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

58

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.

59

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.

The upper zone blood vessels are

periphery of the lower zones (in

of apparent consolidation, indicating alveolar pulmonary edema.

Fig.26 Heart failure following myocardial infarction.

60

Fig.25. Heart failure

he upper zone blood vessels are distended and there are linear densities in the

periphery of the lower zones (interstitial or Kerley‘s B lines) and there are some areas


Heart failure following myocardial infarction.

distended and there are linear densities in the

and there are some areas


Heart failure following myocardial infarction.

61

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

62

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

63

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

64

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

65

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.

66

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.

67

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

68

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).

69

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 2. smoking 3. cholesterol >6,5mmol/L 4. family history of premature cardiovascular disease (women<65y., men - <55 y)

1. reduced HDL cholesterol level 2. raised LDL cholesterol level 3. diabetes mellitus 4. impaired glucose tolerance 5. obesity 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

70

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

Cardiovascular Diseases

Target Organ Damage1 Associated Clinical

Conditions2

I. Used for risk

stratification

-Levels of systolic and

diastolic blood pressure

(Grades 1-3)

-Men >55 years

-Women >65 years

-Smoking

-Total cholesterol >6.5

mmo/l (250 mg/dl)

-Diabetes

-Family history of

premature cardiovascular

disease

II. Other factors adversely

influencing prognosis

-Left ventricular

hypertrophy

(electrocardiogram,

echocardiogram or

radiogram)

-Proteinuria and/or slight

elevation of plasma

creatinine concentration (1.

2 - 2.0 mg/dl)

-Ultrasound or radiological

evidence of atherosclerotic

plaque (carotid, iliac and

femoral arteries, aorta)

-Generalised or focal

narrowing of the retinal

arteries

Cerebrovascular disease

-ischaemic stroke

-cerebral haemorrhage

-transient ischaemic attack

Heart disease

-myocardial infarction

-angina

-coronary revascularisation

-congestive heart failure

Renal disease

-diabetic nephropathy

-renal failure (plasma

creatinine concentration >2.0

mg/dl)

Vascular disease

-dissecting aneurysm

71

-Reduced HDL

cholesterol

-Raised LDL cholesterol

-Microalbuminuria in

diabetes

-Impaired glucose

tolerance

-Obesity

-Sedentary lifestyle

-Raised fibrinogen

-High risk socioeconomic

group

-High risk ethnic group

-High risk geographic

region

-symptomatic arterial disease

Advanced hypertensive

retinopathy

-haemorrhages or exudates

-papilloedema

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

Factors &

Disease History

Grade 1

SBP 140-159 or

DBP 90-99

Grade 2

SBP 160-179 or

DBP 100-109

Grade 3

SBP і 180 or

DBP і 110

I. no other risk

factors

LOW RISK MED RISK HIGH RISK

II. 1-2 risk

factors

MED RISK MED RISK V HIGH RISK

III. 3 or more risk HIGH RISK HIGH RISK V HIGH RISK

72

factors or TOD1

or diabetes

IV. ACC2 V HIGH

RISK

V HIGH

RISK

V HIGH 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.

73

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,

74

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.

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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,

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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.

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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.

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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.

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• 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;

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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

ISCHEMIA

to 30 min

high pointed (coronary) T

wave

PREACUTE

phase

up to 3 days

ST above contour

ACUTE stage to 3 weeks

ST above contour with the transition in (-) T; the formation of pathological Q;

SUBACUTE

stage

to 3 months

ST on the contour, T (-),

pathological Q;

SCAR stage

(final

consolidation of

the scar)

the rest of life ST on the contour, T (-) or

(+), pathological Q

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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.

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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.

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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;

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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.

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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.

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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.

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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;

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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;

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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.

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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:

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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).

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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;

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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.

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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.

Fig.2. The position of the apical four

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

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Fig.1. Mitral incompetence

The position of the apical four-chamber hearts: a color Doppler study of the early


pulmonary veins, left atrium and left ventricle towards the apex of the heart. L

Application

chamber hearts: a color Doppler study of the early


pulmonary veins, left atrium and left ventricle towards the apex of the heart. LV — left

96

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.

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Fig.4. Mitral stenosis

Fig.5.Aortic incompetence

Fig.6. Aortic regurgitation, the severity

of the position of the parasternal long axis of left ventricle. Motley regulatorului flow

begins at the level of closing of the flaps

left atrium, RV — right ventricle, Ao

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Aortic regurgitation, the severity — from small to moderate. Color Doppler study


begins at the level of closing of the flaps of the aortic valve. LV —

right ventricle, Ao — ascending aorta, AR —

Fig.7.Aortic stenosis

from small to moderate. Color Doppler study


— left ventricle, LA —

— aortic regurgitation.

99

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.- 208с.

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.

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