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IN clinical practice determine the following changes in heart sounds:

• change in the volume of the main tones (I and II);
• pathological splitting (bifurcation) of the main tones;
• the appearance of additional tones: pathological III and IV tones, opening tones mitral valve, additional systolic tone (click), pericardial tone and others.

Most often, the causes of the weakening and strengthening of the volume of the main heart sounds are presented in Table. one.

Table 1.

. Splitting of the 1st heart sound. The main reason for the splitting of the first heart sound is the asynchronous closure and fluctuations of the mitral and tricuspid valves. Allocate pathological and physiological splitting.

• Physiological breakdown. In a healthy person, the mitral and tricuspid valves can also close asynchronously, which is accompanied by physiological splitting of the first tone.
• pathological split. Such a situation can arise, for example, with blockade of the right leg of the bundle of His, which leads to a later than normal start of RV contraction and, accordingly, to a later closure of the cuspid valve.

Physiological splitting differs from pathological by significant inconstancy: during deep breath when blood flow to the right side of the heart increases, the tricuspid valve closes a little later, as a result of which splitting of the first tone becomes clearly visible; during exhalation, it decreases or even completely disappears. Pathological splitting of the I tone is longer (more than 0.06 s), and, as a rule, it can be heard on inhalation and exhalation.

Bifurcation and splitting of the II tone , as a rule, is associated with an increase in the duration of RV blood ejection and / or a decrease in LV blood ejection time, which leads, respectively, to a later onset of the pulmonary component and / or an earlier onset of the aortic component of the II tone. Allocate pathological and physiological bifurcation and splitting of the II tone.

• Physiological splitting and bifurcation of the II tone. In healthy young people, unstable physiological splitting of the II tone may occur. It appears at the beginning of inspiration, when blood flow to the right heart and filling of the vessels of the pulmonary circulation increases, which is accompanied by a slight increase in the duration of expulsion of blood from the pancreas and the later appearance of the pulmonary component of the second tone. The filling of the left ventricle on inspiration decreases, since part of the blood is retained in the vessels of the pulmonary circulation. This leads to a slightly earlier occurrence of the aortic component of the II tone.
• Pathological splitting and bifurcation of the II tone. In most cases, it is due to an increase in the duration of expulsion of blood from the pancreas with its pronounced hypertrophy and a decrease in contractility. Pathological bifurcation and splitting of the II tone, in contrast to the physiological splitting, is permanent and persists during inhalation and exhalation.

Pathological III heart sound occurs at the end of the phase fast filling ventricles 0.16-0.20 s after the second tone. It is caused mainly by volume overload of the ventricles and / or increased stiffness of the heart muscle. It most often occurs with systolic heart failure. The appearance of a pathological III tone against the background of tachycardia leads to the formation of a protodiastolic gallop rhythm, which can be heard, for example, in patients with congestive heart failure, acute MI, myocarditis, and others. serious illnesses heart muscle. In these cases, the prognostic value of this auscultatory phenomenon, indicating a sharp drop in ventricular myocardial contractility and the rate of its diastolic relaxation, is extremely high (“a cry of the heart for help”).

In other cases, the appearance of a pathological III tone may only indicate increased stiffness of the ventricular myocardium (for example, in patients with severe hypertrophy or sclerotic changes in the heart muscle).

Pathological IV heart sound occurs during atrial systole and auscultatively resembles a pronounced bifurcation of the first tone. In these cases, a three-term heart rhythm is also determined (presystolic gallop rhythm). Its appearance in an adult indicates, as a rule, a significant increase in end-diastolic pressure in the ventricles of the heart, which is often determined in patients with severe myocardial hypertrophy and impaired diastolic filling of the ventricles, for example, with diastolic CHF. The appearance of AV blockade of the I degree, as a rule, contributes to a better detection of the pathological IV tone.

Systolic gallop - a three-term rhythm that occurs when an additional short tone, or systolic click, appears during the period of ventricular systole (between I and II tones). In most cases, the extra systolic click can be due to one of two things:

The blow of a portion of blood against the compacted wall of the ascending aorta at the very beginning of the period of expulsion of blood from the left ventricle, for example, in patients with atherosclerosis of the aorta or hypertension (in these cases, the so-called early systolic click is recorded, auscultatively resembling splitting of the first tone;

Prolapse of the mitral valve leaflet in the middle or at the end of the exile phase (mesosystolic or late systolic click).

Mitral valve opening tone (click) appears exclusively with stenosis of the left AV foramen at the time of opening of the mitral valve cusps.

Normally, the AV valve leaflets open silently. When the cusps in patients with mitral stenosis at the time of their opening, the initial portion of blood from the LA under the action of a high pressure gradient in the atrium and LV hits the fused valve cusps with great force, which leads to the appearance of a short click. It is better to listen to it at the top of the heart or to the left of the sternum in the IV-V intercostal space; it is separated from the II tone by a short interval (the phase of isovolumic relaxation of the ventricles).

The tone (click) of the opening of the mitral valve, together with the clapping I tone and the II tone accentuated on the pulmonary artery, form a kind of mitral stenosis melody, called the “quail rhythm” and reminiscent of some kind of quail (“sleep-on-ra”).

A.V. Strutynsky
Complaints, history, physical examination

They do not always coincide with the anatomical localization of their sources - valves and the openings they close (Fig. 45). So, the mitral valve is projected at the site of attachment of the III rib to the sternum on the left; aortic - in the middle of the sternum at the level of the III costal cartilages; pulmonary artery - in the II intercostal space on the left at the edge of the sternum; tricuspid valve - in the middle of the line connecting the places of attachment to the sternum of the cartilage of the III left and V right ribs. Such proximity of the valve openings to each other makes it difficult to isolate sound phenomena in the place of their true projection on the chest. In this regard, the places of the best conduction of sound phenomena from each of the valves were determined.

Rice. 45. Projection of the heart valves on the chest:
A - aortic;
L - pulmonary artery;
D, T - two- and three-leaf.

The place of auscultation of the bicuspid valve (Fig. 46, a) is the region of the apical impulse, i.e., the V intercostal space at a distance of 1-1.5 cm medially from the left mid-clavicular line; aortic valve - II intercostal space on the right at the edge of the sternum (Fig. 46, b), as well as the 5th point of Botkin - Erb (the place of attachment of the III-IV rib to the left edge of the sternum; Fig. 46, c); pulmonary valve - II intercostal space on the left at the edge of the sternum (Fig. 46, d); tricuspid valve - the lower third of the sternum, at the base of the xiphoid process (Fig. 46, e).

Rice. 46. ​​Listening to the valves of the heart:
a - bivalve in the apex area;
b, c - aortic, respectively, in the II intercostal space on the right and at the Botkin-Erb point;
g - valve of the pulmonary artery;
d - tricuspid valve;
e - the order of listening to heart sounds.

Listening is carried out in a certain sequence (Fig. 46, e):

1. apex beat area; II intercostal space on the right at the edge of the sternum;
2. II intercostal space on the left at the edge of the sternum;
3. the lower third of the sternum (at the base of the xiphoid process);
4. Botkin - Erb point.

This sequence is due to the frequency of heart valve damage.

The procedure for listening to the valves of the heart:

In practically healthy individuals, when listening to the heart, two tones are usually determined - the first and second, sometimes the third (physiological) and even the fourth.

Normal I and II heart sounds (eng.):

First tone is the sum of the sound phenomena that occur in the heart during systole. Therefore, it is called systolic. It arises as a result of fluctuations of the tense muscle of the ventricles (muscular component), closed cusps of two- and tricuspid valves (valvular component), the walls of the aorta and pulmonary artery in the initial period of blood entering them from the ventricles (vascular component), the atria during their contraction (atrial component).

Formation and components of the I tone (English):

Second tone due to slamming and the resulting fluctuations of the valves of the aorta and pulmonary artery. Its appearance coincides with the beginning of diastole. Therefore, it is called diastolic.

II heart sound (English):

There is a short pause between the first and second tones (no sound phenomena are heard), and the second tone is followed by a long pause, after which the tone reappears. However, beginning students often find it difficult to distinguish between the first and second tones. To facilitate this task, it is recommended to first listen to healthy people with a slow heart rate. Normally, the first tone is heard louder at the apex of the heart and in the lower part of the sternum (Fig. 47, a). This is explained by the fact that sound phenomena from the mitral valve are better carried to the apex of the heart and the systolic tension of the left ventricle is more pronounced than that of the right one. The second tone is heard louder at the base of the heart (in the places of listening to the aorta and pulmonary artery; Fig. 47, b). The first tone is longer and lower than the second.

Rice. 47. Places of the best listening to heart sounds:
a - I tone;
b - II tone.

Listening to obese and thin people alternately, one can be convinced that the volume of heart tones depends not only on the state of the heart, but also on the thickness of the tissues surrounding it. The greater the thickness of the muscle or fat layer, the lower the volume of tones, both the first and the second.

Rice. 48. Determination of the I heart sound by the apex beat (a) and by the pulse of the carotid artery (b).

Heart sounds should be learned to differentiate not only by the relative loudness at the apex and its base, by their different duration and timbre, but also by the coincidence of the appearance of the first tone and pulse on the carotid artery or the first tone and apex beat (Fig. 48). It is impossible to navigate by the pulse on the radial artery, since it appears later than the first tone, especially with a frequent rhythm. Distinguishing the first and second tones is important not only in connection with their independent diagnostic significance, but also because they play the role of sound landmarks for determining noise.

Third tone caused by fluctuations in the walls of the ventricles, mainly the left (with their rapid filling with blood at the beginning of diastole). It is heard with direct auscultation at the apex of the heart or somewhat medially from it, and it is better in the patient's supine position. This tone is very quiet and, in the absence of sufficient auscultation experience, may not be caught. It is heard better in young people (in most cases near the apex beat).

III heart sound (English):

fourth tone is the result of fluctuations in the walls of the ventricles during their rapid filling at the end of diastole due to atrial contraction. Rarely heard.

IV heart sound (English):

You can listen to the tones and murmurs of the heart in normal and pathological conditions on the website

In recent years, phonocardiography has lost its importance as a method of studying the heart. It was replaced and significantly supplemented by echocardiography. However, in order to train students, and even a number of doctors, to assess the sounds heard during the work of the heart, it is necessary

• knowledge of the phase analysis of cardiac activity,
• understanding the origin of tones and noises and
• understanding of PCG and polycardiography.

Unfortunately, doctors often rely on the conclusion of an echocardiologist, shifting responsibility for the diagnosis to him.

1. HEART TONES

During the work of the heart, sounds are produced that are called tones. Unlike musical tones, these sounds consist of the sum of oscillations of different frequencies and amplitudes, i.e. from a physical point of view, they are noise. The only difference between heart sounds and murmurs, which can also occur during the work of the heart, is the brevity of the sound.

During cardiac cycle can occur from two to four heart sounds. The first tone is systolic, the second, third and fourth are diastolic. The first and second tones are always present. The third can be heard in healthy people and in various pathological conditions. The audible fourth tone, with rare exceptions, is pathological. Tones are formed due to fluctuations in the structures of the heart, the initial segments of the aorta and the pulmonary trunk. Phonocardiography made it possible to isolate individual components in the first and second heart sounds. Not all of them are heard directly by the ear or through a stethoscope (phonendoscope). The audible components of the first tone are formed after the closure of the atrioventricular valves, and the second - after the closure of the semilunar valves of the aorta and pulmonary trunk.

Cardiohemic systems. Tones are formed not only due to vibrations of the valve flaps, as it seemed in the past. To designate the complexes of structures, the vibrations of which cause the appearance of tones, R. Rushmer proposed the term cardiohemic systems (Fig. 1.2).

The first tone occurs due to a short-term, but rather powerful vibration of the cardiohemic system of the ventricles (myocardium and atrioventricular valves). The second tone is formed due to oscillations of two cardiohemic systems, consisting of 1) the aortic valve and the aortic root and 2) the pulmonary valve with its initial segment. The cardiohemic system, the vibrations of which form the third and fourth heart sounds, consists of the atria and ventricles with open atrioventricular valves. All cardiohemic systems also include blood located in these structures.

1.1. Origin of tones.

First tone occurs at the very beginning of ventricular systole. It consists of four components (Fig. 1).

First component constitute very weak fluctuations due to asynchronous contraction of the ventricular muscle before the atrioventricular valves close. At this moment, the blood moves towards the atria, causing a tight closure of the valves, somewhat stretching them and bending towards the atria.

Second component. After the atrioventricular valves close, a closed cardiohememic system is formed, consisting of the ventricular myocardium and atrioventricular valves. Due to the elasticity of the valve leaflets, slightly protruding towards the atria, there is a return towards the ventricles, which causes vibrations of the valve leaflets, myocardium and blood in closed system. These fluctuations are quite intense, which makes the second component of the first tone well audible.

Rice. 1. The mechanism of formation of heart sounds according to R. Rushmer. I, II, III- heart sounds. 1-4 - components of the I tone. This figure is placed in the textbooks of Propaedeutics of Internal Diseases with distorted explanations.

Third component. After the mitral valve closes, isometric contraction of the ventricular muscle rapidly raises the intraventricular pressure, which begins to exceed the pressure in the aorta. Blood, rushing towards the aorta, opens the valve, but encounters significant inertial resistance of the blood column in the aorta and stretches its proximal section. This causes a rebound effect and re-oscillation of the cardiohememic system (left ventricle, mitral valve, aortic root, blood). The third component has similar characteristics to the second. The interval between the second and third components is small, and they often merge into one series of oscillations.

Isolation of the muscle and valvular components of the first tone is impractical, because the audible second and third components of the first tone are formed by simultaneous vibrations of both the heart muscle and the atrioventricular valves.

Fourth component due to fluctuations in the aortic wall at the beginning of the ejection of blood from the left ventricle. These are very weak, inaudible vibrations.

Thus, the first tone consists of four successive components. Only the second and third are audible, which usually merge into one sound.

According to A. Luizada, the power of the first tone is only 0.1 provided by vibrations of the valvular apparatus, 0.9 falls on the myocardium and blood. The role of the right ventricle in the formation of a normal first tone is small, since the mass and power of its myocardium are relatively small. However, the right ventricular I tone exists and under certain conditions can be heard.

Second tone.

The initial component of the second tone is represented by several low-frequency vibrations, which are caused by the inhibition of blood flow at the end of systole and its reverse flow in the aorta and pulmonary trunk at the very beginning of ventricular diastole before the closing of the semilunar valves. This inaudible component has no clinical significance and will not be mentioned further. The main components of the second tone are aortic (II A) and pulmonary (II P).

Aortic component of the second tone. At the beginning of the relaxation of the left ventricle, the pressure in it drops sharply. The blood at the root of the aorta rushes towards the ventricle. This movement is interrupted by the rapid closing of the semilunar valve. The inertia of the moving blood stretches the valves and the initial segment of the aorta, and the recoil force creates a powerful vibration of the valve, the walls of the initial part of the aorta and the blood in it.

Pulmonary component of the second tone. It is formed in the pulmonary trunk similarly to the aortic one. Components II A and II P merge into one sound or are heard separately - splitting of the second tone (see Fig. 6).

Third tone.

Relaxation of the ventricles leads to a drop in pressure in them. When it becomes lower than the intra-atrial, the atrioventricular valves open, blood rushes into the ventricles. The inflow of blood into the ventricles that has begun suddenly stops - the phase of rapid filling passes into the phase of slow filling of the ventricles, which coincides with the return to the basal line of the left ventricular pressure curve. A sharp change in blood flow velocity with relaxed walls of the ventricles gives several weak low-frequency oscillations - the third tone. The cardiogemic system (atria, ventricles - their walls and blood in the cavities) cannot give powerful oscillations, since at this moment both the atria and the ventricles are relaxed, therefore, in order to listen to the third left ventricular tone, a number of conditions are important (see 1.5).

Fourth tone (Fig. 2).

At the end of the diastole of the ventricles, the atria contract, starting a new cycle of the heart. The walls of the ventricles are maximally stretched by the blood entering them, which is accompanied by a slight increase in intraventricular pressure. The recoil effect of the stretched ventricles causes a slight oscillation of the cardiohememic system (atria and ventricles with blood enclosed in them). The small intensity of oscillations is due to the fact that tense atria are weak, and powerful ventricles are relaxed. The fourth tone occurs after 0.09-0.12 s from the beginning of the tooth R on the ECG. In healthy people, it is almost never auscultated and is usually not visible on PCG.

Rice. 2. On the left - the mechanism of formation of the fourth heart sound; on the right - a rare case of good recording of the IV tone in a healthy person (observation by I.A. Kassirsky and G.I. Kassirsky);

Thus, during the work of the heart, the formation of four tones is possible.

Two of them have loud, well-audible components. On fig. Figures 4 and 5 show which phases of cardiac activity correspond to heart sounds and their components.

1.2. Mechanism mitral valve closure.

The convergence of the mitral valve leaflets begins during atrial systole due to a drop in pressure between them, due to the rapid blood flow. An abrupt cessation of atrial systole with continued blood flow leads to an even greater drop in pressure between the leaflets, which causes almost complete valve closure, which is also facilitated by the formation of vortices in the ventricle, pressing the leaflets from the outside (Fig. 3). Thus, by the beginning of the ventricular systole, the mitral orifice is almost completely closed, therefore, asynchronous contraction of the ventricles does not cause regurgitation, but quickly “seals” the atrioventricular orifice, creating conditions for powerful oscillations of the cardiohememic system (the second and third components of the first tone).

Rice. 3. The mechanism of closing the mitral valve according to R. Rushmer (writing in the text).

1.3. Phases of cardiac activity (Fig. 4, 5).

The cardiac cycle is divided into systole and diastole according to contraction and relaxation of the ventricles. In this case, atrial systole occurs at the very end of ventricular diastole (presystole).

Ventricular systole consists of four phases. At the beginning of systole, the atrioventricular valves are open, and the semilunar valves of the aorta and pulmonary trunk are closed. The phase of isometric contraction of the ventricles begins when all four valves are closed, but at the end of its semilunar valves open, although there is still no blood flow to the aorta and pulmonary trunk (3rd component of tone I, see Fig. 1). The expulsion of blood occurs in two phases - fast and slow.

Rice. 4. Phases of cardiac activity. 1 - QI tone = asynchronous contraction phase, 2 - isometric contraction phase, 3 - ejection phase, 4 - protodiastolic interval, 5 - isometric relaxation phase, 6 - fast filling phase, 7 - slow filling phase, 8 - protodiastole, 9 - mesodiastole . 10 - presystole, OMC - opening of the mitral valve.

The ventricular diastole is divided into three parts:

• protodiastole, which ends with the opening (normally silent) of the atrioventricular valves;
• mesodiastole - from the opening of the atrioventricular valves to atrial systole and
• presystole - from the beginning of atrial contraction to the Q or R wave (in the absence of a Q wave) on the ECG.

In the clinical literature, the division of both systole and diastole into approximately equal parts continues without regard to physiological phases, which is difficult to agree with. If for systole this does not contradict anything and is convenient for indicating where the pathological sound is located (early systole, mesosystole, late systole), then for diastole this is unacceptable, because. causes confusion: the III tone and the mesodiastolic murmur of mitral stenosis are incorrectly in the protodiastole, instead of the mesodiastole. Hence the incorrect names: protodiastolic gallop (I, II, pathological III tone) instead of mesodiastolic (see 1.5), protodiastolic murmur of mitral stenosis instead of mesodiastolic.

Rice. 5. Phases of cardiac activity, heart sounds. The duration of the phases is given at a heart rate of »75/min. Closed valves are shown in black circles, open valves are shown in light circles. The arrows indicate the opening or closing of the valves during a phase (horizontal arrows) or during a phase change (vertical arrows). On the right, Roman numerals mark the tones, Arabic numerals mark the components of the first tone; IIA and IIP are the aortic and pulmonary components of the II tone, respectively.

1.4. Characteristics of normal heart sounds.

The first and second heart sounds are usually, even in pathological conditions, are heard over the entire precordial region, but their assessment is carried out at the place of formation. The main parameters of tones are loudness (intensity), duration and pitch (frequency response). It is also necessary to note the presence or absence of splitting of the tone and its special features (for example, clapping, ringing, metallic, etc. These features are called the nature of the tones). The doctor usually compares the first and second tones at each auscultation point, but he must, and this is a more difficult task, compare the tone heard with its due characteristic at this point in a healthy person with the same age, body weight and physique as the patient.

Loudness and pitch. The absolute loudness of tones depends on many reasons, including those not related to the heart itself. This includes the physical and emotional state of a person, physique, degree of muscle development chest and subcutaneous fat, body temperature, etc. Therefore, when assessing the volume of a tone, many points must be taken into account. For example, the muffled tones in an obese person are a completely natural phenomenon, as is the increase in tones during fever.

It is necessary to take into account the unequal perception by the human ear of sounds of the same intensity, but different heights. There is something called "subjective loudness". The ear is much less sensitive to very low and very high sounds. Sounds with a frequency in the range of 1000-2000 hertz are best perceived. Heart sounds are very complex sounds made up of many vibrations of varying frequency and intensity. In the first tone, low-frequency components predominate, in the second - high-frequency components. In addition, with strong pressure on the skin with a stethoscope, it stretches and, becoming a membrane, dampens low and enhances high-frequency components. The same happens when using an instrument with a membrane. Therefore, the second tone is often perceived as louder than it really is. If on FCG in a healthy person, when recording from the apex of the heart, the first tone always has a larger amplitude than the second, then when listening, one may get the impression that their volume is the same. And yet, more often the first tone at the apex is louder and lower than the second, and on the aorta and pulmonary trunk the second tone is louder and higher than the first.

tone duration. This parameter cannot be assessed by ear. Although the first FCG tone is usually longer than the second, the audible components may be the same.

Splitting of normal heart sounds. Two loud components of the first tone usually merge into one sound, however, the interval between them can reach a significant value (30-40 ms), which is already caught by the ear as two close sounds, i.e., as a splitting of the first tone. It does not depend on breathing and is constantly heard directly by the ear or through a stethoscope with a funnel of small diameter (even better through a hard stethoscope), if it is not pressed strongly against the patient's body. Cleavage is heard only at the apex of the heart.

The time interval between the closure of the mitral and tricuspid valves is normally small, usually 10-15 milliseconds, i.e. the cardiohememic systems of both ventricles fluctuate almost simultaneously, therefore, in healthy people, there is no reason for splitting the first tone, due to a slight lag of the right ventricular first tone from the left ventricular one , especially since the power of the right ventricular tone is negligible in comparison with the left ventricular tone.

Splitting of the second tone in the area of ​​the pulmonary artery is heard quite often. The interval between the aortic and pulmonary components increases during inspiration, so splitting is well heard at the height of inspiration or at the very beginning of exhalation during two to three cardiac cycles. Sometimes it is possible to trace the entire sound dynamics: an unsplit second tone, slight splitting during inhalation, when the interval II A -II P is barely caught; a gradual increase in the interval to the height of inspiration and again the convergence of components II A and II P and a continuous tone from the second third or middle of exhalation (see Fig. 6).

The splitting of the second tone during inspiration is due to the fact that due to

negative intrathoracic pressure, the thin-walled right ventricle is more filled with blood, its systole ends later, and therefore, at the beginning of ventricular diastole, the pulmonary valve closes much later than the aortic valve. Splitting is not auscultated with very frequent and shallow breathing, tk. at the same time there are no hemodynamic changes leading to splitting.

This phenomenon is heard especially well in young persons with a thin chest wall during quiet deep breathing. When listening to the pulmonary trunk in healthy people, the frequency of splitting the second tone is about 100% in children, 60% in patients under 30 years of age, and 35% in people over 50 years of age.

1.5. Tone changes.

Changing the volume of tones.

During auscultation of the heart, an increase or decrease in both tones can be noted, which may be due both to the peculiarities of the conduction of sounds from the heart to the auscultation point on the chest wall, and to the actual change in the volume of tones.

Violation of the conduction of sounds and, consequently, weakening of tones is observed with a thick chest wall (a large mass of muscles or a thick layer of fat, edema) or when the heart is pushed away from the anterior chest wall (exudative pericarditis, pleurisy, emphysema). Strengthening of tones, on the contrary, occurs with a thin chest wall, in addition, with fever, after physical exertion, with excitement, thyrotoxicosis, if there is no heart failure.

The weakening of both tones associated with the pathology of the heart, is observed with a decrease in myocardial contractility, regardless of the cause.

A change in the volume of one of the tones is usually associated with pathology of the heart and blood vessels. The weakening of the I tone is observed with non-hermetic closure of the mitral and aortic valves (the period of closed valves is absent both in mitral and aortic insufficiency), with a slowdown in the contraction of the left ventricle (myocardial hypertrophy, myocarditis, heart failure, myocardial infarction, complete blockade left bundle branch, hypothyroidism), as well as with bradycardia and p-Q lengthening.

It is known that the volume of the I tone depends on the degree of divergence of the mitral valve leaflets at the beginning of the ventricular systole. With a large discrepancy between them, there is a greater deflection of the valves in the period of closed valves towards the atria, there is also a greater return towards the ventricles and a more powerful oscillation of the cardiohememic system. Therefore, I tone becomes weaker with increase in p-Q and increases with p-Q shortening.

Strengthening of the I tone is mainly due to an increase in the rate of increase in intraventricular pressure, which is observed with a decrease in its filling during diastole (mitral stenosis, extrasystole).

The main reasons for the weakening of the II tone on the aorta are: violation of the tightness of the closure of the semilunar valve (insufficiency of the aortic valve), with a decrease in blood pressure, as well as with a decrease in the mobility of the valves (valvular aortic stenosis).

AccentIItones. It is estimated by comparing the volume of the II tone in the II intercostal space at the edge of the sternum, respectively, on the right or left. The accent is noted where the II tone is louder, and may be on the aorta or on the pulmonary trunk. Accent II tone can be physiological and pathological.

The physiological emphasis is age related. On the pulmonary trunk, it is heard in children and adolescents. It is usually explained by a closer location of the pulmonary trunk to the site of auscultation. On the aorta, the accent appears by the age of 25-30 and somewhat intensifies with age due to the gradual thickening of the aortic wall.

You can talk about a pathological accent in two situations:

1. when the accent does not correspond to the proper auscultation point for age (for example, a loud II sound on the aorta in a young man) or
2. when the volume of the II tone is greater at a point, although corresponding to age, but it is too high in comparison with the volume of the II tone in a healthy person of the same age and physique, or the II tone has a special character (ringing, metallic).

The reason for the pathological accent of the II tone on the aorta is an increase in blood pressure and (or) sealing of the valve leaflets and the aortic wall. Emphasis of II tone on the pulmonary trunk is usually observed with pulmonary arterial hypertension(mitral stenosis, cor pulmonale, left ventricular failure, Aerza's disease).

Pathological splitting of heart sounds.

A distinct splitting of the I heart sound can be heard with blockade of the right leg of the His bundle, when excitation is carried out much earlier to the left ventricle than to the right one, therefore the right ventricular first tone noticeably lags behind the left ventricular one. At the same time, splitting of the first tone is better heard in right ventricular hypertrophy, including in patients with cardiomyopathy. This sound picture resembles the systolic gallop rhythm (see below).

With pathological splitting of the II tone, the interval II A - II P ³ 0.04 s, sometimes reaches 0.1 s. The split may be of the normal type, i.e. increase on inspiration, fixed (independent of breathing) and paradoxical when II A comes after II P. Paradoxical splitting can be diagnosed only with the help of a polycardiogram, including ECG, PCG and carotid sphygmogram, the incisura on which coincides with II A.

Three-term (three-stroke) rhythms.

Rhythms in which, in addition to the main I and II tones, additional tones (III or IV, mitral valve opening tone, etc.) are heard, are called three-membered, or three-stroke.

A three-term rhythm with a normal third tone is often heard in young healthy people, especially after exercise in a position on the left side. III tone has a normal characteristic (quiet and low - deaf) and should not cause suspicion of pathology. Often the third tone is heard in patients with a healthy heart who have anemia.

gallop rhythms. Pathological third tone is observed in violation of the contractility of the myocardium of the left ventricle (heart failure, myocardial infarction, myocarditis); with an increase in volume and atrial hypertrophy (mitral defects); with any increase in the diastolic tone of the ventricles or their diastolic rigidity (pronounced hypertrophy or cicatricial changes in the myocardium, as well as with peptic ulcer).

A three-term rhythm with a weakened I tone and a pathological III tone was called the proto-diastolic gallop rhythm, because. with tachycardia, it resembles the sound of a galloping horse's hooves. However, it should be noted that the III tone is in the mesodiastole, i.e. we are talking about the mesodiastolic gallop rhythm (see Fig. 4.5).

The presystolic gallop rhythm is due to the appearance of the IV tone, when IV, I and II tones are successively heard. It is observed in patients with a significant decrease in ventricular myocardial contractility (heart failure, myocarditis, myocardial infarction), or with severe hypertrophy (stenosis of the aortic orifice, hypertonic disease, cardiomyopathy, Fig. 7).

Fig.7. Loud IV tone in a patient with hypertrophic cardiomyopathy. The upper FKG curve, on the low-frequency channel (middle curve) vibrations of IV and I tones practically merge, at medium frequencies they are clearly separated. During auscultation, the presystolic gallop rhythm was heard, the IV tone was determined by palpation.

Summative gallop is observed in the presence of III and IV tones, which merge into one additional tone.

A systolic gallop is heard when an additional tone appears after the I tone. It may be due to a) the impact of a blood stream on the aortic wall at the very beginning of the period of exile (aortic stenosis, see Fig. 16; hypertension, atherosclerosis) - this is an early systolic click or b) prolapse of the mitral valve leaflet into the atrial cavity (late systolic click, it appears in the middle or at the end of the ejection phase).

quail rhythm. With mitral stenosis, the opening of the mitral valve is often heard, which resembles a click. It often occurs after 0.7-0.11 s from the beginning of the second tone (the earlier, the higher the pressure in the left atrium). Presystolic murmur, clapping I tone, II tone and an additional tone of mitral valve opening - all this resembles the singing of a quail: “ss-pat-po-ra”.

Pericardial tone with adhesive pericarditis, it is explained by a sudden cessation of ventricular filling due to pericardial fusion - a shell that limits further increase in volume. It is very similar to the opening click of the mitral valve or the third tone. Diagnosis is carried out by a complex of symptoms, both clinical and obtained using instrumental methods.

In conclusion of the first part of "Auscultation of the Heart", dedicated to heart sounds, it should be noted:

We listen and evaluate short sounds - tones that occur during the work of the heart, not valves. To assess the tones, three auscultation points are sufficient.

Diastole is divided into protodiastole, mesodiastole and presystole.

physiological mechanisms of the heart, and not by dividing it into 3 equal parts.

The first phonendoscopes were sheets of paper folded into a tube or hollow bamboo sticks, and many doctors used only their own hearing organ. But they all wanted to hear what was happening inside the human body, especially when it comes to such an important organ as the heart.

Heart sounds are sounds that are formed during the contraction of the walls of the myocardium. Normally, a healthy person has two tones, which may be accompanied by additional sounds, depending on which pathological process develops. A doctor of any specialty must be able to listen to these sounds and interpret them.

Cardiac cycle

The heart beats at a rate of sixty to eighty beats per minute. This, of course, is an average value, but ninety percent of the people on the planet fall under it, which means that you can take it as the norm. Each beat consists of two alternating components: systole and diastole. The systolic heart sound, in turn, is divided into atrial and ventricular. In time, it takes 0.8 seconds, but the heart has time to contract and relax.

Systole

As mentioned above, there are two components involved. First, there is atrial systole: their walls contract, blood enters the ventricles under pressure, and the valve flaps slam shut. It is the sound of closing valves that is heard through the phonendoscope. This entire process takes 0.1 seconds.

Then comes the systole of the ventricles, which is a much more complex work than it happens with the atria. First, note that the process lasts three times longer - 0.33 seconds.

The first period is the tension of the ventricles. It includes phases of asynchronous and isometric contractions. It all starts with the fact that the eclectic impulse spreads through the myocardium, It excites individual muscle fibers and causes them to spontaneously contract. Because of this, the shape of the heart changes. Due to this, the atrioventricular valves close tightly, increasing the pressure. Then there is a powerful contraction of the ventricles, and the blood enters the aorta or pulmonary artery. These two phases take 0.08 seconds, and in the remaining 0.25 seconds, blood enters the great vessels.

Diastole

Here, too, everything is not as simple as it might seem at first glance. The relaxation of the ventricles lasts 0.37 seconds and occurs in three stages:

1. Proto-diastolic: after the blood has left the heart, the pressure in its cavities decreases, and the valves leading to the large vessels close.
2. Isometric relaxation: the muscles continue to relax, the pressure drops even more and equalizes with the atrial. This opens the atrioventricular valves, and blood from the atria enters the ventricles.
3. Filling of the ventricles: fluid fills the lower ventricles along the pressure gradient. When the pressure equalizes, the blood flow gradually slows down, and then stops.

Then the cycle repeats again, starting with systole. Its duration is always the same, but diastole can be shortened or lengthened depending on the speed of the heartbeat.

The mechanism of formation of I tone

No matter how strange it may sound, but 1 heart sound consists of four components:

1. Valve - he is the leader in the formation of sound. In fact, these are fluctuations of the cusps of the atrioventricular valves at the end of ventricular systole.
2. Muscular - oscillatory movements of the walls of the ventricles during contraction.
3. Vascular - stretching of the walls at the moment when blood enters them under pressure.
4. Atrial - atrial systole. This is the immediate beginning of the first tone.

The mechanism of formation of II tone and additional tones

So, the 2nd heart sound includes only two components: valvular and vascular. The first is the sound that arises from the blows of blood on the valves of the artia and the pulmonary trunk at the moment when they are still closed. The second, that is, the vascular component, is the movements of the walls of large vessels when the valves finally open.

In addition to the two main ones, there are also 3 and 4 tones.

The third tone is the fluctuations of the ventricular myocardium during diastole, when blood passively drains into an area of ​​lower pressure.

The fourth tone appears at the end of systole and is associated with the end of the expulsion of blood from the atria.

Characteristics of the first tone

Heart sounds depend on many causes, both intra- and extracardiac. The sonority of 1 tone depends on the objective state of the myocardium. So, first of all, the volume is provided by the tight closure of the heart valves and the speed with which the ventricles contract. Such features as the density of the cusps of the atrioventricular valves, as well as their position in the cavity of the heart, are considered secondary.

It is best to listen to the first heart sound at its apex - in the 4th-5th intercostal space to the left of the sternum. For more accurate coordinates, it is necessary to percussion the chest in this area and clearly define the boundaries of cardiac dullness.

Characteristic II tone

To listen to him, you need to put the bell of the phonendoscope over the base of the heart. This point is located slightly to the right of the xiphoid process of the sternum.

The volume and clarity of the second tone also depends on how tightly the valves close, only now semilunar. In addition, the speed of their work, that is, the closing and oscillation of the risers, affects the reproduced sound. And additional qualities are the density of all structures involved in the formation of tone, as well as the position of the valves during the expulsion of blood from the heart.

Rules for listening to heart sounds

The sound of the heart is probably the most peaceful in the world, after white noise. Scientists have a hypothesis that it is he who hears the child in the prenatal period. But in order to identify damage to the heart, just listening to how it beats is not enough.

First of all, you need to do auscultation in a quiet and warm room. The posture of the examined person depends on which valve needs to be listened to more carefully. This can be a lying position on the left side, vertically, but with the body tilted forward, on the right side, etc.

The patient should breathe rarely and shallowly, and at the request of the doctor, hold his breath. In order to clearly understand where the systole is and where the diastole is, the doctor must, in parallel with listening, palpate the carotid artery, the pulse on which completely coincides with the systolic phase.

Order of auscultation of the heart

After a preliminary determination of absolute and relative cardiac dullness, the doctor listens to the heart sounds. It starts, as a rule, from the top of the organ. The mitral valve is clearly audible. Then they move on to the valves of the main arteries. First, to the aortic - in the second intercostal space to the right of the sternum, then to the pulmonary artery - at the same level, only on the left.

The fourth point to listen to is the base of the heart. It is located at the base but can move to the sides. So the doctor must check what is the shape of the heart, and the electrical axis to accurately listen

Auscultation is completed at the Botkin-Erb point. Here you can hear She is in the fourth intercostal space on the left side of the sternum.

Additional tones

The sound of the heart does not always resemble rhythmic clicks. Sometimes, more often than we would like, it takes bizarre forms. Doctors have learned to identify some of them only by listening. These include:

Mitral valve click. It can be heard near the apex of the heart, it is associated with organic changes in the valve leaflets and appears only with acquired heart disease.

Systolic click. Another type of mitral valve disease. In this case, its valves do not close tightly and, as it were, turn outward during systole.

Perekardton. Found in adhesive pericarditis. Associated with excessive stretching of the ventricles due to the mooring formed inside.

Rhythm quail. Occurs with mitral stenosis, manifested by an increase in the first tone, an accent of the second tone on the pulmonary artery and a click of the mitral valve.

gallop rhythm. The reason for its appearance is a decrease in myocardial tone, appears against the background of tachycardia.

Extracardiac causes of amplification and weakening of tones

The heart beats in the body throughout life, without interruption and rest. So, when it wears out, outsiders appear in the measured sounds of its work. The reasons for this can be either directly related to damage to the heart, or not depend on it.

Strengthening tones contribute to:

Cachexia, anorexia, thin chest wall;

Atelectasis of the lung or part of it;

Tumor in the posterior mediastinum, moving the lung;

Infiltration of the lower lobes of the lungs;

Bullae in the lungs.

Decreased heart sounds:

Excessive weight;

The development of the muscles of the chest wall;

subcutaneous emphysema;

The presence of fluid in the chest cavity;

Intracardiac causes of amplification and weakening of heart sounds

Heart sounds are clear and rhythmic when the person is at rest or asleep. If he began to move, for example, climbed the stairs to the doctor's office, then this can cause an increase in heart sound. Also, the acceleration of the pulse can be caused by anemia, diseases endocrine system etc.

A muffled heart sound is heard with acquired heart defects, such as mitral or aortic stenosis, valve insufficiency. Aortic stenosis contributes to the divisions close to the heart: the ascending part, the arch, the descending part. Muffled heart sounds are associated with an increase in myocardial mass, as well as with inflammatory diseases of the heart muscle, leading to dystrophy or sclerosis.

Heart murmurs

In addition to tones, the doctor can hear other sounds, the so-called noises. They are formed from the turbulence of the flow of blood that passes through the cavities of the heart. Normally, they shouldn't be. All noise can be divided into organic and functional.

1. Organic ones appear when anatomical, irreversible changes in the valve system occur in the organ.
2. Functional noises are associated with impaired innervation or nutrition of the papillary muscles, an increase in heart rate and blood flow velocity, and a decrease in its viscosity.

Murmurs may accompany heart sounds or may be independent of them. Sometimes when inflammatory diseases superimposed on the heartbeat, and then you need to ask the patient to hold his breath or lean forward and auscultate again. This simple trick will help you avoid mistakes. As a rule, when listening to pathological noises, they try to determine in which phase of the cardiac cycle they occur, to find the place of the best listening and to collect the characteristics of the noise: strength, duration and direction.

Noise Properties

According to the timbre, several types of noise are distinguished:

Soft or blowing (usually not associated with pathology, often in children);

Rough, scraping or sawing;

Musical.

According to the duration, they are distinguished:

Short;

Long;

By volume:

loud;

Descending;

Increasing (especially with narrowing of the left atrioventricular orifice);

Increasing-decreasing.

The change in volume is recorded during one of the phases of cardiac activity.

Height:

High-frequency (with aortic stenosis);

Low-frequency (with mitral stenosis).

There are some general patterns in auscultation of noises. Firstly, they are well heard in the locations of the valves, due to the pathology of which they were formed. Secondly, the noise radiates in the direction of blood flow, and not against it. And thirdly, like heart sounds, pathological murmurs are best heard where the heart is not covered by the lungs and is tightly attached to the chest.

It is better to listen in the supine position, because the blood flow from the ventricles becomes easier and faster, and diastolic - sitting, because under gravity, the fluid from the atria enters the ventricles faster.

Murmurs can be differentiated by their localization and the phase of the cardiac cycle. If the noise in the same place appears both in systole and in diastole, then this indicates a combined lesion of one valve. If, in systole, noise appears at one point, and in diastole - at another, then this is already a combined lesion of two valves.

Characteristics of heart sounds.

The opening of the valves is not accompanied by distinct fluctuations, i.e. almost silently, and the closure is accompanied by a complex auscultatory picture, which is regarded as I and II tones.

Itone occurs when the atrioventricular valves (mitral and tricuspid) close. Louder, longer lasting. This is a systolic tone, as it is heard at the beginning of systole.

IItone It is formed when the semilunar valves of the aorta and pulmonary artery close.

Itone called systolic and according to the mechanism of formation consists of 4 components:

main component- valvular, represented by amplitude oscillations resulting from the movement of the mitral and tricuspid valve cusps at the end of diastole and the beginning of systole, and the initial oscillation is observed when the mitral valve cusps are closed, and the final oscillation is observed when the tricuspid valve cusps are closed, therefore, the mitral and tricuspid components are isolated;

muscle component– low-amplitude oscillations are superimposed on high-amplitude oscillations of the main component ( isometric ventricular tension, appears in about 0.02 sec. to the valve component and layered on it); and also arise as a result asynchronous ventricular contractions during systole, i.e. as a result of contraction of the papillary muscles and the interventricular septum, which ensure the slamming of the cusps of the mitral and tricuspid valves;

vascular component- low-amplitude oscillations that occur at the time of opening of the aortic and pulmonary valves as a result of vibration of the walls of the aorta and pulmonary artery under the influence of blood flow moving from the ventricles to the main vessels at the beginning of the ventricular systole (exile period). These oscillations occur after the valve component after about 0.02 seconds;

atrial component- low-amplitude oscillations resulting from atrial systole. This component precedes the valvular component of the I tone. It is detected only in the presence of mechanical atrial systole, disappears with atrial fibrillation, nodal and idioventricular rhythm, AV blockade (lack of atrial excitation wave).

IItone called diastolic and occurs as a result of the slamming of the cusps of the semilunar valves of the aorta and pulmonary artery. They begin diastole and end systole. Consists of 2nd components:

valve component occurs as a result of the movement of the valves of the semilunar valves of the aorta and pulmonary artery at the moment of their slamming;

vascular component associated with the vibration of the walls of the aorta and pulmonary artery under the influence of the flow of blood directed towards the ventricles.

When analyzing heart tones, it is necessary to determine them quantity, find out what tone is first. With a normal heart rate, the solution to this problem is clear: I tone occurs after a longer pause, i.e. diastole, II tone - after after a short pause, i.e. systole. With tachycardia, especially in children, when systole is equal to diastole, this method is not informative and the following technique is used: auscultation in combination with palpation of the pulse on the carotid artery; the tone that coincides with the pulse wave is I.

In adolescents and young people with a thin chest wall and a hyperkinetic type of hemodynamics ( increased speed and an increase in strength, with physical and mental stress) additional III and IV tones (physiological) appear. Their appearance is associated with the fluctuation of the walls of the ventricles under the influence of blood moving from the atria to the ventricles during ventricular diastole.

IIItone - protodiastolic, because appears at the beginning of diastole immediately after the II tone. It is best heard with direct auscultation at the apex of the heart. It is a weak, low, short sound. It is a sign of good development of the myocardium of the ventricles. With an increase in ventricular myocardial tone in the phase of rapid filling in ventricular diastole, the myocardium begins to oscillate and vibrate. Auscultated through 0.14 -0.20 after the II tone.

IV tone - presystolic, because appears at the end of diastole, precedes the I tone. Very quiet, short sound. It is heard in individuals with increased ventricular myocardial tone and is due to fluctuations in the ventricular myocardium when blood enters them in the atrial systole phase. More often heard in a vertical position in athletes and after emotional stress. This is due to the fact that the atria are sensitive to sympathetic influences, therefore, with an increase in the tone of the sympathetic NS, there is some lead in atrial contractions from the ventricles, and therefore the fourth component of the I tone begins to be heard separately from the I tone and is called the IV tone.

FeaturesIAndIItones.

I tone is heard louder at the apex and on the tricuspid valve at the base of the xiphoid process at the beginning of systole, that is, after a long pause.

II tone is heard louder at the base - II intercostal space on the right and left at the edge of the sternum after a short pause.

I tone is longer, but lower, duration 0.09-0.12 sec.

II tone is higher, shorter, duration 0.05-0.07 sec.

The tone that coincides with the apex beat and with the pulsation of the carotid artery is tone I, tone II does not match.

I tone does not coincide with the pulse on the peripheral arteries.

Auscultation of the heart is performed at the following points:

the region of the apex of the heart, which is determined by the localization of the apex beat. At this point, a sound vibration is heard that occurs during the operation of the mitral valve;

II intercostal space, to the right of the sternum. Here the aortic valve is heard;

II intercostal space, to the left of the sternum. Here the pulmonary valve is auscultated;

region of the xiphoid process. The tricuspid valve is heard here

point (zone) Botkin-Erbe(III-IV intercostal space 1-1.5 cm lateral (to the left) from the left edge of the sternum. Here, sound vibrations are heard that occur during the operation of the aortic valve, less often - mitral and tricuspid.

During auscultation, the points of maximum sounding of heart tones are determined:

I tone - the area of ​​\u200b\u200bthe apex of the heart (I tone is louder than II)

II tone - the region of the base of the heart.

The sonority of the II tone is compared to the left and right of the sternum.

In healthy children, adolescents, young people of asthenic body type, there is an increase in the II tone on the pulmonary artery (quieter on the right than on the left). With age, there is an increase in the II tone above the aorta (II intercostal space on the right).

On auscultation, analyze sonority heart tones, which depends on the summation effect of extra- and intracardiac factors.

TO extracardiac factors include the thickness and elasticity of the chest wall, age, body position, and the intensity of pulmonary ventilation. Sound vibrations are better conducted through a thin elastic chest wall. Elasticity is determined by age. In the vertical position, the sonority of heart tones is greater than in the horizontal position. At the height of inhalation, sonority decreases, while exhalation (as well as during physical and emotional stress) it increases.

Extracardiac factors include pathological processes of extracardiac origin, for example, with a tumor of the posterior mediastinum, with a high standing of the diaphragm (with ascites, in pregnant women, with obesity of the middle type), the heart “presses” more against the anterior chest wall, and the sonority of heart sounds increases.

The sonority of the heart tones is influenced by the degree of airiness of the lung tissue (the size of the air layer between the heart and the chest wall): with increased airiness of the lung tissue, the sonority of the heart tones decreases (with emphysema), with a decrease in the airiness of the lung tissue, the sonority of the heart tones increases (with wrinkling of the lung tissue, surrounding the heart).

With cavitary syndrome, heart tones can acquire metallic shades (sonority increases) if the cavity is large and the walls are tense.

The accumulation of fluid in the pleural streak and in the pericardial cavity is accompanied by a decrease in the sonority of heart tones. In the presence of air cavities in the lung, pneumothorax, accumulation of air in the pericardial cavity, an increase in the gas bubble of the stomach and flatulence, the sonority of heart tones increases (due to the resonance of sound vibrations in the air cavity).

TO intracardiac factors, which determines the change in the sonority of heart tones in a healthy person and in extracardiac pathology, refers to the type of cardiohemodynamics, which is determined by:

the nature of neurovegetative regulation of cardio-vascular system in general (the ratio of the tone of the sympathetic and parasympathetic divisions of the ANS);

the level of physical and mental activity of a person, the presence of diseases that affect the central and peripheral link of hemodynamics and the nature of its neurovegetative regulation.

Allocate 3 types of hemodynamics:

eukinetic (normokinetic). The tone of the sympathetic division of the ANS and the tone of the parasympathetic division of the ANS are balanced;

hyperkinetic. The tone of the sympathetic division of the ANS predominates. Characterized by an increase in the frequency, strength and speed of contraction of the ventricles, an increase in the speed of blood flow, which is accompanied by an increase in the sonority of heart tones;

hypokinetic. The tone of the parasympathetic division of the ANS predominates. There is a decrease in the sonority of heart tones, which is associated with a decrease in the strength and speed of contraction of the ventricles.

The tone of the ANS changes during the day. During the active time of the day, the tone of the sympathetic division of the ANS increases, and at night - the parasympathetic division.

With heart disease intracardiac factors include:

change in the speed and strength of contractions of the ventricles with a corresponding change in the speed of blood flow;

a change in the speed of movement of the valves, depending not only on the speed and strength of contractions, but also on the elasticity of the valves, their mobility and integrity;

leaf travel distance - distance from ?????? before?????. Depends on the size of the diastolic volume of the ventricles: the larger it is, the shorter the run distance, and vice versa;

the diameter of the valve opening, the condition of the papillary muscles and the vascular wall.

A change in I and II tones is observed with aortic defects, with arrhythmias, with violations of AV conduction.

With aortic insufficiency the sonority of the II tone decreases at the base of the heart and the I tone - at the top of the heart. The decrease in sonority of the second tone is associated with a decrease in the amplitude of the valvular apparatus, which is explained by a defect in the valves, a decrease in their surface area, as well as incomplete closure of the valves at the time of their slamming. Reducing sonorityItones associated with a decrease in valvular oscillations (oscillation - amplitude) of tone I, which is observed with severe dilatation of the left ventricle in aortic insufficiency (the aortic opening expands, relative mitral insufficiency develops). The muscle component of tone I also decreases, which is associated with the absence of a period of isometric tension, because there is no period of complete closure of the valves.

With aortic stenosis a decrease in the sonority of I and II tones in all auscultatory points is associated with a significant decrease in the movement of blood flow, which, in turn, is due to a decrease in the rate of contraction (contractility?) of the ventricles working against the narrowed aortic valve. With atrial fibrillation and bradyarrhythmia, an uneven change in the sonority of tones occurs, associated with a change in the duration of diastole and with a change in the diastolic volume of the ventricle. With an increase in the duration of diastole, blood volume increases, which is accompanied by a decrease in the sonority of heart tones in all auscultatory points.

With bradycardia diastolic overload is observed, therefore, a decrease in the sonority of heart tones in all auscultatory points is characteristic; with tachycardia diastolic volume decreases and the sound rises.

With pathology of the valvular apparatus an isolated change in the sonority of I or II tone is possible.

With stenosis,AVblockadeAVarrhythmias the sonority of the I tone increases.

With mitral stenosis I tone flapping. This is due to an increase in the diastolic volume of the left ventricle, and since. the load falls on the left ventricle, there is a discrepancy between the force of contractions of the left ventricle and the volume of blood. There is an increase in the distance run, tk. BCC decreases.

With a decrease in elasticity (fibrosis, Sanoz), the mobility of the valves decreases, which leads to sonority reductionItones.

With complete AV blockade, which is characterized by a different rhythm of atrial and ventricular contractions, a situation may arise when the atria and ventricles contract simultaneously - in this case, there is sonority increaseItones at the top of the heart - Strazhesko's "cannon" tone.

Isolated sonority attenuationItones observed with organic and relative mitral and tricuspid insufficiency, which is characterized by a change in the cusps of these valves (past rheumatism, endocarditis) - deformation of the cusps, which causes incomplete closure of the mitral and tricuspid valves. As a result, a decrease in the amplitude of the oscillations of the valvular component of the first tone is observed.

With mitral insufficiency, the oscillations of the mitral valve decrease, therefore sonority decreasesItones at the apex of the heart, and with tricuspid - on the basis of the xiphoid process.

Complete destruction of the mitral or tricuspid valve leads to extinctionItones - at the top of the heart,IItones - in the region of the base of the xiphoid process.

Isolated changeIItones in the region of the base of the heart is observed in healthy people, with extracardiac pathology and pathology of the cardiovascular system.

Physiological change II tone ( amplification of sonority) above pulmonary artery observed in children, adolescents, young people, especially during exercise (physiological increase in pressure in the ICC).

In older people amplification of sonorityIIsounds over the aorta associated with an increase in pressure in the BCC with a pronounced compaction of the walls of blood vessels (atherosclerosis).

AccentIIsounds over the pulmonary artery observed in the pathology of external respiration, mitral stenosis, mitral insufficiency, decompensated aortic disease.

Weakening sonorityIItones over the pulmonary artery is determined with tricuspid insufficiency.

Change in the volume of heart sounds. They can occur in amplification or weakening, it can be simultaneously for both tones or in isolation.

Simultaneous weakening of both tones. Causes:

1. extracardiac:

Excessive development of fat, mammary gland, muscles of the anterior chest wall

Effusive left-sided pericarditis

Emphysema

2. intracardial - a decrease in the contractility of the ventricular myocardium - myocardial dystrophy, myocarditis, myocardiopathy, cardiosclerosis, pericarditis. A sharp decrease in myocardial contractility leads to a sharp weakening of the first tone, in the aorta and LA the volume of incoming blood decreases, which means that the second tone weakens.

Simultaneous volume boost:

Thin chest wall

Wrinkling of lung edges

Increasing the standing of the diaphragm

Volumetric formations in the mediastinum

Inflammatory infiltration of the edges of the lungs adjacent to the heart, as dense tissue conducts sound better.

The presence of air cavities in the lungs located near the heart

An increase in the tone of the sympathetic NS, which leads to an increase in the rate of myocardial contraction and tachycardia - emotional arousal, after heavy physical exertion, thyrotoxicosis, in initial stage arterial hypertension.

GainItones.

Mitral stenosis - flapping I tone. The volume of blood at the end of diastole in the left ventricle decreases, which leads to an increase in the rate of myocardial contraction, and the leaflets of the mitral valve thicken.

Tachycardia

Extrasystole

Atrial fibrillation, tachy form

Incomplete AV blockade, when the P-th contraction coincides with the F-s contraction - Strazhesko's cannon tone.

WeakeningItones:

Mitral or tricuspid valve insufficiency. The absence of p-yes closed valves leads to a sharp weakening of the valve and muscle component

Aortic valve insufficiency - more blood enters the ventricles during diastole - increased preload

Stenosis of the aortic orifice - I tone weakens due to severe hypertrophy of the LV myocardium, a decrease in the rate of myocardial contraction due to the presence of increased afterload

Diseases of the heart muscle, accompanied by a decrease in myocardial contractility (myocarditis, dystrophy, cardiosclerosis), but if cardiac output decreases, then II tone also decreases.

If at the top of the I tone in volume it is equal to the II or louder than the II tone - weakening of the I tone. I tone is never analyzed on the basis of the heart.

Volume changeIItones. The pressure in the LA is less than the pressure in the aorta, but the aortic valve is located deeper, so the sound above the vessels is the same in volume. In children and in people under 25 years of age, there is a functional increase (accent) of the II tone over LA. The reason is a more superficial location of the LA valve and a higher elasticity of the aorta, lower pressure in it. With age, blood pressure in the BCC increases; LA moves backward, the accent of the second tone over LA disappears.

Reasons for amplificationIIsounds over the aorta:

Increase in blood pressure

Atherosclerosis of the aorta, due to sclerotic compaction of the valves, an increase in the II tone above the aorta appears - toneBittorf.

Reasons for amplificationIItones over LA- increased pressure in the BCC with mitral heart disease, chronic respiratory diseases, primary pulmonary hypertension.

WeakeningIItones.

Above the aorta: - insufficiency of the aortic valve - the absence of a closing period (?) of the valve

Aortic stenosis - as a result of a slow increase in pressure in the aorta and a decrease in its level, the mobility of the aortic valve decreases.

Extrasystole - due to a shortening of diastole and a small cardiac output of blood into the aorta

Severe arterial hypertension

Reasons for weakeningIItones on LA– insufficiency of LA valves, stenosis of the LA mouth.

Splitting and bifurcation of tones.

In healthy people, there is asynchronism in the work of the right and left ventricles in the heart, normally it does not exceed 0.02 seconds, the ear does not catch this time difference, we hear the work of the right and left ventricles as single tones.

If the time of asynchronism increases, then each tone is perceived not as a single sound. On FKG it is registered within 0.02-0.04 sec. Bifurcation - a more noticeable doubling of tone, asynchronism time 0.05 sec. and more.

The reasons for the bifurcation of tones and splitting are the same, the difference is in time. Functional bifurcation of tone can be heard at the end of exhalation, when intrathoracic pressure rises and blood flow from the ICC vessels to the left atrium increases, resulting in increased blood pressure on the atrial surface of the mitral valve. This slows down its closure, which leads to the auscultation of splitting.

Pathological bifurcation of the I tone occurs as a result of a delay in the excitation of one of the ventricles during the blockade of one of the legs of the His bundle, this leads to a delay in the contraction of one of the ventricles or with ventricular extrasystole. Severe myocardial hypertrophy. One of the ventricles (more often the left - with aortic hypertension, aortic stenosis) myocardium is excited later, more slowly reduced.

BifurcationIItones.

Functional bifurcation is more common than the first, occurs in young people at the end of inhalation or the beginning of exhalation, during exercise. The reason is the non-simultaneous end of the systole of the left and right ventricles. Pathological bifurcation of the II tone is more often noted on the pulmonary artery. The reason is the increase in pressure in the IWC. As a rule, amplification of the II tone on the LH is accompanied by a bifurcation of the II tone on the LA.

Additional tones.

In systole, additional tones appear between I and II tones, this, as a rule, a tone, which is called a systolic click, appears with prolapse (sagging) of the mitral valve due to prolapse of the mitral valve leaflet during systole into the LA cavity - a sign of connective tissue dysplasia. It is often heard in children. The systolic click may be early or late systolic.

In diastole during systole, III pathological tone appears, IV pathological tone and the tone of the opening of the mitral valve. IIIpathological tone occurs after 0.12-0.2 sec. from the beginning of the II tone, that is, at the beginning of diastole. Can be heard at any age. It occurs in the phase of rapid filling of the ventricles in the event that the myocardium of the ventricles has lost its tone, therefore, when the cavity of the ventricle is filled with blood, its muscle easily and quickly stretches, the wall of the ventricle vibrates, and a sound is produced. Auscultated in severe myocardial damage (acute myocardial infections, severe myocarditis, myocardial dystrophy).

PathologicalIVtone occurs before tone I at the end of diastole in the presence of crowded atria and a sharp decrease in ventricular myocardial tone. The rapid stretching of the wall of the ventricles that have lost their tone, when a large volume of blood enters them in the atrial systole phase, causes myocardial fluctuations and an IV pathological tone appears. III and IV tones are heard better at the apex of the heart, on the left side.

gallop rhythm first described by Obraztsov in 1912 - "a cry of the heart for help". It is a sign of a sharp decrease in myocardial tone and sharp decrease contractility of the ventricular myocardium. So named because it resembles the rhythm of a galloping horse. Signs: tachycardia, weakening of I and II tone, the appearance of pathological III or IV tone. Therefore, a protodiastolic (three-part rhythm due to the appearance of the III tone), presystolic (III tone at the end of diastole about the IV pathological tone), mesodiastolic, summative (with severe tachycardia, III and IV tones merge, are heard in the middle of diastole summation III tone).

Mitral valve opening tone- a sign of mitral stenosis, appears after 0.07-0.12 seconds from the beginning of the second tone. With mitral stenosis, the leaflets of the mitral valve are fused together, forming a kind of funnel through which blood from the atria enters the ventricles. When blood flows from the atria into the ventricles, the opening of the mitral valve is accompanied by a strong tension of the valves, which contributes to the appearance of a large number of vibrations that form sound. Together with a loud, clapping I tone, II tone on the LA forms "quail rhythm" or mitral stenosis melody, best heard at the apex of the heart.

pendulumrhythm- a heart melody is relatively rare, when both phases are balanced due to diastole and the melody resembles the sound of a swinging clock pendulum. In more rare cases with a significant decrease in myocardial contractility, systole may increase and the pop duration becomes equal to diastole. It is a sign of a sharp decrease in myocardial contractility. Heart rate can be anything. If the pendulum rhythm is accompanied by tachycardia, this indicates embryocardia, that is, the melody resembles the heartbeat of a fetus.