A change in heart sounds can primarily be expressed in a weakening or strengthening of the sonority of one or both of them, in a change in timbre, duration, in their splitting or bifurcation, in some cases - in the appearance of additional tones. In this case, determining the place of best listening to pathological sound phenomena is of diagnostic importance. Strengthening of the second tone in the 2nd intercostal space on the left speaks of its emphasis on the pulmonary artery (determined by comparing its volume and timbre on the pulmonary artery and aorta). This indicates an increase in pressure in the pulmonary circulation, which can be observed in diseases of the heart, as well as the respiratory system (mitral defects, emphysema, pneumosclerosis, chronic pneumonia). Strengthening of the second tone in the 2nd intercostal space on the right indicates its emphasis on the aorta, which is observed with an increase in blood pressure in the systemic circulation (arterial hypertension), as well as in the case of hardening of the wall and valve of the aorta in atherosclerosis and a number of other diseases.

Strengthening the first sound at the apex of the heart most often occurs with narrowing of the left atrioventricular orifice (mitral stenosis), tachycardia. This is due to the fact that with this defect, during diastole, less blood flows into the left ventricle than normal, and it contracts more quickly (transition from a relaxed to a tense state). In addition, with mitral stenosis, the timbre of the first tone changes due to vibrations of the sclerotic cusps of the mitral valve. It takes on a crackling tone, reminiscent of the sound of a flag flapping in the wind. This sound at the apex of the heart with mitral stenosis is called “popping”.

Intensity of tone I (English):

Weakening of the first sound at the apex of the heart can be observed during inflammatory processes of its muscles (myocarditis), cardiosclerosis (scar changes in the heart muscle), and damage to the valve apparatus (bicuspid and tricuspid, as well as aortic).

Weakening of the second sound on the aorta possible with aortic defects (aortic valve insufficiency or stenosis of its mouth).

Weakening of the second tone on the pulmonary artery occurs when the valve is insufficient or its opening is narrowed (stenosis).

If during auscultation of the heart, instead of one of the tones, two short ones are heard, following each other after a short period of time, then this indicates split tone. If the difference in the time of occurrence of these components is insignificant and there is no impression of bifurcation, we are talking about tone splitting. Thus, there is no fundamental qualitative difference between bifurcation and splitting of tones. There is only some quantitative difference: splitting is the initial phase, and bifurcation is a more pronounced degree of disruption of the unity of tones.

Bifurcation and splitting of tones can be physiological and pathological. For example, the bifurcation of the first tone may depend on the non-simultaneous closure of the bicuspid and tricuspid valves as a result of changes in pressure in the chest during different phases of breathing. But more often, a split in the first tone indicates pathological changes in the heart. It occurs, as a rule, when one of the legs of the atrioventricular bundle (bundle of His) is blocked, which leads to non-simultaneous contraction of the right and left ventricles of the heart. This can occur with significant blockade of the atrioventricular (atrioventricular) node, with sclerosis of the initial part of the aorta.

Physiologically split I tone (English):

Forked I tone (English):

In case of severe heart damage, a three-part rhythm can be heard. It is caused by weakening of the myocardium (inflammation, degenerative changes, toxic lesions) of the left ventricle and occurs as a result of rapid stretching of its walls under the pressure of blood flowing from the atrium. This creates a melody of a three-part rhythm (first, second and additional third tones), reminiscent of the clatter of a galloping horse - “ gallop rhythm" It is also figuratively called the “cry of the heart for help,” since it is a sign of severe heart damage. The rhythm of the gallop is best heard directly by the ear (along with the sound, a slight impulse is perceived, transmitted from the heart to the chest in the diastole phase) in the area of ​​the apex of the heart or the third-fourth intercostal space on the left. It can be heard especially clearly when the patient is lying on his left side. But this creates inconvenience for direct listening with the ear. In such cases, a phonendoscope is used.

There are protodiastolic, mesodiastolic and presystolic gallop rhythms (depending on the diastole phase, during which the pathological third sound appears).

gallop rhythm an auscultatory finding of three (triple r.) or four (quadruple r.) heart sounds; the extra sounds occur in diastole and are related either to atrial contraction (S), to early rapid filling of a ventricle (S), or to concurrence of both events (summation gallop) .

Translation:
gallop rhythm heard as a three-membered or four-membered rhythm. Additional sounds appear in diastole and are caused either by atrial contraction, or early rapid filling of the ventricle, or a combination of both mechanisms (summation gallop).

Summation gallop:

Quadruple rhythm (English):

Much more common are bifurcation and splitting of the second tone, caused by non-simultaneous closure of the pulmonary artery and aortic valves due to increased pressure in the pulmonary or systemic circulation. Bifurcation and splitting of the second tone can also be physiological and pathological.

Physiological splitting of the second tone is heard exclusively at the base of the heart during inhalation and exhalation or during physical activity. At the end of a deep inhalation, when the chest expands due to a decrease in pressure in it, the blood is somewhat retained in the dilated vessels of the small circle and therefore enters in less quantity into the left atrium, and from there into the left ventricle. The latter, due to less blood filling, ends systole earlier than the right one, and the closure of the aortic valve precedes the closure of the pulmonary valve. During exhalation, the opposite conditions are created. In the case of increased pressure in the chest, blood, as if squeezed out of the vessels of the pulmonary circle, enters in large quantities into the left part of the heart, and the systole of the left ventricle, and therefore the beginning of its diastole, occurs later than the right.

Paradoxical splitting of the second tone (English):

Pathological bifurcation of the second tone (English):

Fixed splitting of the 2nd tone (English):

At the same time, a split second tone may be a sign of serious pathological changes in the heart and its valves. Thus, a bifurcation of the second sound at the base of the heart (second intercostal space on the left) is heard with mitral stenosis. This is due to the fact that the hypertrophied and blood-filled right ventricle ends systole later than the left. Therefore, the aortic component of the second sound occurs earlier than the pulmonary one. Bifurcation or splitting of the second sound in bicuspid valve insufficiency is associated with greater blood filling of the left ventricle than normal, which leads to prolongation of its systole, and the diastole of the left ventricle begins later than the right. Because of this, the aortic valve closes later than the pulmonary valve.

One should distinguish from the true splitting of the second tone its sound melody, which only superficially resembles splitting. An example is the additional tone that occurs during the opening of the bicuspid (mitral) valve with mitral stenosis. It has a high-pitched clicking tone and is perceived as a loud echo following the second tone. The additional tone, together with the clapping first and second, form a peculiar melody, reminiscent of the cry of a quail. Hence the name of this sound phenomenon, heard with mitral stenosis at the apex of the heart, “ quail rhythm" Its distribution area is extensive - from the apex of the heart up and into the axillary fossa.

Sometimes, when listening to the heart, against the background of rare and dull tones, a lonely, very loud tone appears, the so-called "cannon tone" Strazhesko. It is caused by the simultaneous contraction of the atria and ventricles, which is observed with complete atrioventricular block, i.e. when impulses from the atria do not reach the ventricles and they each contract in their own rhythm (the atria contract more often), but in some cycle their contractions coincide.

Tones of exile (English):

All heart sounds (English):

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

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

• knowledge of 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 echocardiography specialist, shifting responsibility for the diagnosis to him.

1. HEART SOUND

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

During the cardiac cycle, two to four heart sounds may occur. The first sound is systolic, the second, third and fourth are diastolic. The first and second tones are always there. The third can be heard in healthy people and in various pathological conditions. An audible fourth tone, with rare exceptions, is pathological. Tones are formed due to vibrations of the structures of the heart, the initial segments of the aorta and pulmonary trunk. Phonocardiography made it possible to identify 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 the vibrations of the valve flaps, as was thought in the past. To designate complexes of structures whose vibrations cause the appearance of tones, R. Rushmer proposed the term cardiohemic systems (Fig. 1,2).

The first tone occurs due to short-term, but quite powerful vibration of the cardiohemic system of the ventricles (myocardium and atrioventricular valves). The second tone is formed due to vibrations of two cardiohemic systems, consisting of 1) the aortic valve and aortic root and 2) the pulmonary valve with its initial segment. The cardiohemic system, the oscillations 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 caused by asynchronous contraction of the ventricular muscles before the closure of the atrioventricular valves. At this moment, the blood moves towards the atria, causing the valves to close tightly, stretching them somewhat and bending towards the atria.

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

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

Third component. After mitral valve closure, isometric tension of the ventricular muscle rapidly increases 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 repeated oscillation of the cardiohemic 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.

Isolating the muscle and valve 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 caused by vibrations of the aortic wall at the beginning of blood ejection from the left ventricle. These are very weak, inaudible vibrations.

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

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

Second tone.

The initial component of the second tone is represented by several low-frequency vibrations, which are caused by 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 closure 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. As the left ventricle begins to relax, its pressure drops sharply. The blood located in the aortic root rushes towards the ventricle. This movement is interrupted by the rapid closure of the semilunar valve. The inertia of 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 located in it.

Pulmonary component of the second tone. It is formed in the pulmonary trunk similarly to the aortic. 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 intraatrial valve, the atrioventricular valves open and blood rushes into the ventricles. The blood flow into the ventricles that has begun suddenly stops - the rapid filling phase passes into the slow ventricular filling phase, which coincides with a return to the basal line of the left ventricular pressure curve. A sharp change in the speed of blood flow with relaxed walls of the ventricles gives several weak low-frequency oscillations - the third tone. The cardiohemic system (atria, ventricles - their walls and blood in the cavities) cannot give powerful oscillations, since at this moment both the atria and ventricles are relaxed, therefore, in order to listen to the third left ventricular sound, a number of conditions are important (see 1.5).

Fourth tone (Fig. 2).

At the end of ventricular diastole, the atria contract, beginning a new cycle of cardiac activity. 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 stretched ventricles causes a slight oscillation of the cardiohemic system (atria and ventricles with blood enclosed in them). The low intensity of oscillations is due to the fact that the tense atria are low-power, and the powerful ventricles are relaxed. The fourth tone occurs 0.09-0.12 s from the beginning of the wave R on the ECG. In healthy people, it is almost never heard and is usually not visible on FCG.

Rice. 2. On the left – the mechanism of formation of the fourth heart sound; on the right – a rare case of good registration 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, easily audible components. In Fig. 4 and 5 show which phases of cardiac activity the heart sounds and their components correspond to.

1.2. Mechanism closure of the mitral valve.

The rapprochement of the mitral valve leaflets begins during atrial systole due to a drop in pressure between them caused by the rapid flow of blood. 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 closure of the valve, 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 ventricular systole, the mitral orifice is almost completely closed, so asynchronous contraction of the ventricles does not cause regurgitation, but quickly “seals” the atrioventricular orifice, creating conditions for powerful oscillations of the cardiohemic system (the second and third components of the first sound).

Rice. 3. The mechanism of mitral valve closure 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 the 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 it the semilunar valves open, although there is still no blood flow into the aorta and pulmonary trunk (3rd component of the first sound, see Fig. 1). Expulsion of blood occurs in two phases - fast and slow.

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

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, both systole and diastole continue to be divided into approximately equal parts without taking into account the 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 third tone and mesodiastolic murmur of mitral stenosis are incorrectly found in protodiastole, instead of 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. Black circles show closed valves, light circles show open ones. 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 indicate tones, Arabic numerals indicate components of the first tone; IIA and IIP are the aortic and pulmonary components of tone II, respectively.

1.4. Characteristics of normal heart sounds.

The first and second heart sounds are usually, even in pathological conditions, heard over the entire atrial region, but they are assessed at the site of formation. The main parameters of tones are volume (intensity), duration and pitch (frequency response). The presence or absence of tone splitting and its special features (for example, clapping, ringing, metallic, etc.) are also necessarily noted. These features are called the nature of the tones. The physician usually compares the first and second sounds at each point of auscultation, but he must, and this is a more difficult task, compare the auscultated tone with its proper characteristic at a given point in a healthy person with the same age, body weight and physique as the patient.

Volume and pitch of tones. The absolute volume 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, the degree of development of the chest muscles and subcutaneous fat, body temperature, etc. Therefore, when assessing the volume of a tone, many points must be taken into account. For example, muffled tones in an obese person are a completely natural phenomenon, just like increased 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 significantly 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 frequencies and intensities. In the first tone, low-frequency components predominate, in the second, high-frequency components predominate. In addition, when strong pressure is applied to the skin with a stethoscope, it stretches and, becoming a membrane, dampens low-frequency components and enhances high-frequency components. The same thing happens when using a tool with a membrane. Therefore, the second tone is often perceived as louder than it actually is. If on FCG in a healthy person, when recording from the apex of the heart, the first tone always has a greater amplitude than the second, then when listening, one may get the impression that their volume is the same. And yet, more often the first sound at the apex is louder and lower than the second, and on the aorta and pulmonary trunk the second sound is louder and higher than the first.

Duration of tones. This parameter cannot be assessed by ear. Although the first tone on a PCG is usually longer than the second, their audible components may be the same.

Splitting of normal heart sounds. Two loud components of the first tone usually merge into one sound, but the interval between them can reach a significant value (30-40 ms), which is already perceived 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 small-diameter funnel (even better through a rigid stethoscope), if it is not pressed tightly against the patient’s body. Splitting 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 cardiohemic systems of both ventricles fluctuate almost simultaneously, therefore in healthy people there is no reason for splitting the first sound, due to a slight lag of the right ventricular first sound from the left ventricular one , especially since the power of the right ventricular tone is negligible in comparison with the left ventricular tone.

The 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 the splitting is well heard at the height of inspiration or at the very beginning of expiration for two to three cardiac cycles. Sometimes it is possible to trace all the sound dynamics: an unsplit second tone, a slight split during inhalation, when the interval II A -II P is barely perceptible; 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 filled more with blood, its systole ends later, and therefore, at the beginning of ventricular diastole, the pulmonary valve closes significantly later than the aortic valve. The splitting is not heard with very frequent and shallow breathing, because in this case, hemodynamic changes leading to splitting do not occur.

This phenomenon is especially well heard in young people 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 old, and 35% in people over 50 years old.

1.5. Changes in tones.

Changing the Volume of Tones.

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

Impaired conduction of sounds and, consequently, weakening of tones is observed when the chest wall is thick (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). Intensification 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.

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. Weakening of the first tone is observed when the cusps of the mitral and aortic valves are not tightly closed (the period of closed valves is absent in both mitral and aortic insufficiency), when the contraction of the left ventricle is slowed down (myocardial hypertrophy, myocarditis, heart failure, myocardial infarction, complete blockade of the left bundle branch His, hypothyroidism), as well as with bradycardia and prolongation of p-Q.

It is known that the volume of the first sound depends on the degree of divergence of the mitral valve leaflets at the beginning of ventricular systole. With a large divergence, there is a greater deflection of the valves in the period of closed valves towards the atria, a greater recoil towards the ventricles and a more powerful oscillation of the cardiohemic system are observed. Therefore, the I tone becomes weaker as p-Q increases and strengthens as p-Q shortens.

Strengthening of the first 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 second sound in the aorta are: violation of the tightness of the closure of the semilunar valve (aortic valve insufficiency), with a decrease in blood pressure, as well as with a decrease in the mobility of the valves (valvular aortic stenosis).

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

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

We can talk about a pathological accent in two situations:

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

The reason for the pathological emphasis of the second tone on the aorta is an increase in blood pressure and (or) compaction of the valve leaflets and the aortic wall. An emphasis on the second tone on the pulmonary trunk is usually observed in pulmonary arterial hypertension (mitral stenosis, cor pulmonale, left ventricular failure, Aerza disease).

Pathological splitting of heart sounds.

A distinct splitting of the first heart sound can be heard during right bundle branch block, when excitation is carried out significantly earlier to the left ventricle than to the right, so the right ventricular first sound is noticeably behind the left ventricular one. In this case, the splitting of the first tone is better heard in cases of right ventricular hypertrophy, including in patients with cardiomyopathy. This sound pattern resembles the systolic rhythm of a gallop (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 splitting may be of the normal type, i.e. increase on inspiration, fixed (independent of breathing) and paradoxical when II A appears after II P. Paradoxical splitting can be diagnosed only with the help of a polycardiogram, including an ECG, PCG and carotid sphygmogram, the incisura on which coincides with II A.

Three-part (three-beat) rhythms.

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

A three-part rhythm with a normal third tone is often heard in young healthy people, especially after physical activity in a position on the left side. The third tone has a normal characteristic (quiet and low - dull) and should not raise suspicion of pathology. Often the third sound is heard in patients with a healthy heart who have anemia.

Gallop rhythms. A pathological third tone is observed when the contractility of the left ventricular myocardium is impaired (heart failure, myocardial infarction, myocarditis); with an increase in volume and hypertrophy of the atria (mitral defects); with any increase in the diastolic tone of the ventricles or their diastolic rigidity (severe hypertrophy or cicatricial changes in the myocardium, as well as with peptic ulcer disease).

The three-part rhythm with a weakened 1st tone and a pathological 3rd tone is called the protodiastolic gallop rhythm, because with tachycardia, it resembles the clatter of the hooves of a galloping horse. However, it should be noted that the third tone is in the mesodiastole, i.e. we are talking about the mesodiastolic gallop rhythm (see Fig. 4.5).

The presystolic gallop rhythm is caused by the appearance of the IV tone, when the 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 (aortic stenosis, hypertension, cardiomyopathy, Fig. 7).

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

A summation 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 first sound. It can be caused by a) the impact of a stream of blood on the aortic wall at the very beginning of the ejection period (aortic stenosis, see Fig. 16; hypertension, atherosclerosis) - this is an early systolic click or b) prolapse of the mitral valve leaflet into the atrium cavity (late systolic click, it appears in the middle or at the end of the expulsion phase).

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

Pericardial tone in adhesive pericarditis, it is explained by the sudden cessation of ventricular filling due to the pericardial adhesion, an armor that limits further increase in volume. It is very similar to the mitral valve opening click or third sound. Diagnosis is carried out based on a set 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 - the sounds that arise from the heart, not the valves. Three auscultation points are sufficient to evaluate tones.

Diastole is divided into protodiastole, mesodiastole and presystole, taking into account

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

First tone occurs during systole after a long pauses. It is best heard at the apex of the heart, since the systolic tension of the left ventricle is greater than that of the right.

The nature the first tone is longer and lower than the second.

Second tone formed during diastole after a short pauses. It is best heard at the base of the heart, as it occurs when the semilunar leaflets of the aortic valves and pulmonary trunk close. Unlike the first tone, it shorter duration and higher.

In pathology, when the sonority of tones can change, it helps to distinguish the first and second tones by the fact that the first tone coincides with the apex beat(if the latter is palpable) and with the pulse of the aorta and carotid artery.

Changes in heart sounds can be expressed as:

v weakening or enhancing the sonority of one or both tones,

v in changing their timbre, duration,

v in the appearance of bifurcation or splitting of fundamental tones,

v the appearance of additional tones.

Heart sounds are intensifying when large air cavities are located near it (large pulmonary cavity, large gas bubble of the stomach) - due to resonance. The sonority of the tones also depends on the composition of the blood flowing through the heart: when the viscosity of the blood decreases, as is observed with anemia, the sonority of the tones increases.

Fig. 8. Valve projection locations

on the anterior chest wall

In the diagnosis of heart diseases

It is of great importance to identify changes in tones caused by damage to the heart itself, i.e. caused by cardiac causes.

Weakening both tones can be observed with a decrease in the contractility of the heart muscle in patients with myocarditis, myocardial dystrophy, cardiosclerosis, with collapse, accumulation of fluid in the pericardial cavity.

Gain Both tones arise due to an increase in the influence of the sympathetic nervous system on the heart. This is observed during heavy physical work, anxiety, and in people suffering from Graves' disease.

More often than a change in both heart sounds, there is a change in one of them, which is especially important in the diagnosis of heart disease.

Weakening of the first toneat the top heart observed:

· Insufficiency of the mitral and aortic valves.

With mitral valve insufficiency during systole, the valve leaflets do not completely cover the left atrioventricular orifice.

Gain first tone at the top heart observed:

· with narrowing of the mitral orifice.

Weakening of the first toneat the base of the xiphoid process of the sternum

· with insufficiency of the tricuspid valve and the pulmonary valve.

Gain first tone base of the xiphoid process of the sternum is heard:

· with stenosis of the right atrioventricular orifice.

An increase in the first tone is also observed with extrasystole– premature contraction of the heart - due to low diastolic filling of the ventricles.

Fine, second tone strength above the aorta and pulmonary trunk is the same.

Weakening of the second tone above the aorta is observed:

· at aortic insufficiency valves, or due to their cicatricial compaction;

· with large destruction of the aortic valve leaflets, the second sound above it may not be heard at all;

· with a significant decrease in blood pressure;

Weakening of the second toneabove the pulmonary the trunk is observed:

· in case of insufficiency of its valve (which is extremely rare);

· with a decrease in pressure in the pulmonary circulation.

Strengthening the second tone may be noted either above the aorta or above the pulmonary trunk.

In cases where the second tone is more sonorous above the aorta, they speak of the accent of the second tone on the aorta, but if it is more sonorous above the pulmonary trunk, they speak of the accent of the second tone on the pulmonary artery.

Accent of the second tone on the aorta observed:

· when the pressure in it increases (hypertension, nephritis, heavy physical work, mental agitation), since at the beginning of diastole the blood hits the valve flaps with greater force.

Emphasis of the second tone on the pulmonary artery appears:

· with increased pressure in the pulmonary circulation, blood overflow of the pulmonary vessels (for example, with mitral heart defects),

· obstruction of blood circulation in the lungs and narrowing of the pulmonary artery bed (with emphysema, pneumosclerosis, etc.)

Heart murmurs.

When auscultating the heart, in some cases, in addition to tones, sound phenomena called heart murmurs are heard.

Murmurs can occur: inside the heart itself - intracardial, outside of it, extracardiac.

Organic noises- occur due to anatomical changes in the structure of the heart valves.

Functional noise– appear:

in case of dysfunction of unchanged valves

· with an increase in blood flow speed or a decrease in blood viscosity.

The most common cause of intracardial murmur is heart defects.

According to the time of noise appearance during systole or diastole differentiate between systolic and diastolic murmurs.

Systolic murmur appears:

· when, during systole, blood, moving from one part of the heart to another or from the heart to large vessels, encounters a narrowing on its way.

· with stenosis of the aortic mouth or pulmonary trunk, since with these defects, during the expulsion of blood from the ventricles, an obstacle arises in the path of blood flow - narrowing of the vessel.

· listened to insufficiency of the mitral and tricuspid valves.

Its occurrence is explained by the fact that during ventricular systole, blood flows not only into the aorta and pulmonary trunk, but also back into the atrium through an incompletely covered mitral or tricuspid opening. Since this not completely covered hole is a narrow gap, noise occurs when blood passes through it.

Diastolic murmur appears in cases where there is a narrowing in the path of blood flow in diastole phase:

· with narrowing of the left or right atrioventricular orifice, since with these defects during diastole there is a narrowing in the path of blood flow from the atria to the ventricles.

· in case of insufficiency of the aortic valve, pulmonary trunk - due to reverse blood flow from the vessels into the ventricles through the gap formed when the leaflets of the altered valve are not completely closed.

During auscultation it is necessary to determine:

1) the ratio of noise to the phase of cardiac activity (to systole or diastole);

2) properties of noise, its nature, strength, duration;

3) noise localization, i.e. best place to listen;

The ratio of noise to systole or diastole is determined by the same criteria by which we distinguish between the first and second sounds.

When assessing heart sounds, you should try to listen separately to each component of the cardiac cycle: the 1st sound and the systolic interval, and then the 2nd sound and the diastolic interval.

The sound of heart sounds can change under the influence of various reasons. Normally, heart sounds are clear. They can gradually weaken, becoming muffled or dull (obesity, hypertrophy of the chest muscles, emphysema, fluid accumulation in the pericardial cavity, severe myocarditis) or intensify (asthenics, people with a thin chest, tachycardia).

The first sound is formed as a result of vibrations of the cusps of the mitral and tricuspid valves when they close, as well as vibrations of the myocardium itself and large vessels.

Therefore, the 1st tone consists of three components:

Valvular (closing of the mitral and tricuspid valves), giving the main contribution to the intensity of 1 tone;

Muscular, associated with vibrations of the heart muscle during isometric contraction of the ventricles;

Vascular, caused by vibrations of the walls of the aorta and pulmonary artery at the beginning of the expulsion period.

The 1st sound is assessed at the apex of the heart, where in a healthy person it is always louder, longer than the 2nd tone and lower in frequency. It coincides with the apical impulse and pulsation of the carotid arteries.

Factors that determine the intensity of the 1st tone include:

The position of the valves at the beginning of systole,

The tightness of the ventricular chamber during the period of isovolumetric contraction (closeness of the valves),

Valve closing speed

Mobility of the valves,

The speed (but not the strength!) of ventricular contraction (the value of the end-diastolic volume of the ventricles, the thickness of the myocardium, the intensity of metabolism in the myocardium);

It follows that the higher the valve closing speed, the louder the 1st tone will be (amplification of 1 tone). So, with tachycardia, when the filling of the ventricles is reduced and the amplitude of movement of the valves increases, the 1st tone will be loud. When an extrasystole appears, the 1st sound intensifies (Strazhesko's cannon tone) due to the low diastolic filling of the ventricles. With mitral stenosis, due to fusion and thickening of the valve leaflets, which slam quickly and loudly, 1 tone will also be amplified (slamming 1 tone).

Weakening of the 1st sound can occur with ventricular dilatation (mitral and aortic valve insufficiency); damage to the heart muscle (myocarditis, cardiosclerosis), with bradycardia (due to increased filling of the ventricles and a decrease in the amplitude of oscillation of the heart muscle).

Vibrations of the valve flaps of the aorta and pulmonary artery at the moment of their closure and the walls of the supravalval sections of the aorta and pulmonary artery lead to the appearance of a 2nd tone, therefore, this tone consists of 2 components - valvular and vascular. The quality of its sound is assessed only on the basis of the heart, where it is louder, shorter and higher than the 1st tone and follows after a short pause.

The assessment of the second tone is carried out by comparing the intensity of its sound on the aorta and pulmonary artery.

Normally, the second sound in the aorta and pulmonary artery sounds the same. If it sounds louder in the second intercostal space on the right, then they speak of an emphasis of the 2nd tone on the aorta, and if in the second intercostal space on the left - an emphasis of the 2nd tone on the pulmonary artery. The reason for the accentuation is most often an increase in pressure in the systemic or pulmonary circulation. When the cusps of the aortic valve or pulmonary artery are fused or deformed (with rheumatic heart defects, infective endocarditis), a weakening of the second tone occurs over the affected valve.

Splitting and bifurcation of tones. Heart sounds consist of several components, but upon auscultation they are heard as one sound, because The human hearing organ is not capable of perceiving two sounds separated by an interval of less than 0.03 seconds. If the valves do not close simultaneously, then during auscultation two components of the 1st or 2nd tones will be heard. If the distance between them is 0.04 - 0.06 seconds, then this is called splitting, if more than 0.06 s - bifurcation.

For example, a split first sound is often heard with right bundle branch block due to the fact that the right ventricle begins to contract later and the tricuspid valve closes later than normal. With blockade of the left bundle branch, the bifurcation of the 1st sound is heard much less frequently, since the delay in the oscillation of the mitral component coincides in time with the delay in the tricuspid component.

There is a physiological splitting/bifurcation of the second tone, which does not exceed 0.06 seconds. and appears only during inspiration, which is associated with a prolongation of the period of blood expulsion by the right ventricle due to an increase in its filling during inspiration. It should be emphasized that the pulmonary component of the second sound is often heard in a limited area: in the 2nd – 4th intercostal space along the left edge of the sternum, so it can only be assessed in this area.

In diseases accompanied by a significant increase in pressure in the pulmonary or systemic circulation (stenosis or insufficiency of the mitral valve, some congenital heart defects), a pathological split in the second tone occurs, which is clearly audible both on inhalation and exhalation.

In addition to the main heart sounds (1st and 2nd), the physiological 3rd and 4th sounds can also be heard normally. These are low-frequency tones that arise when the walls of the ventricles (usually the left) vibrate as a result of passive (III sound) and active (IV) filling. Physiological muscle tones are found in children (up to 6 years old - IV tone), adolescents, young people, mostly thin, under the age of 25 years (III tone). The appearance of the third sound is explained by the active expansion of the left ventricle during its rapid filling at the beginning of systole. It is heard at the apex of the heart and at the fifth point.

In patients with damage to the heart muscle, pathological 3rd and 4th heart sounds are heard, which are usually combined with a weakening of the sonority of the 1st tone above the apex and tachycardia, therefore a so-called gallop rhythm is formed. Since the third sound is recorded at the beginning of diastole, it is called the protodiastolic gallop rhythm. The pathological IV tone occurs at the end of diastole and is called the presystolic gallop rhythm.

When auscultating additional heart sounds, it should be remembered that muscle tones are difficult to hear through the membrane, so it is better to use a “bell” to auscultate them.

Extratons. In addition to muscle tones, an additional sound can be heard in diastole - the opening tone of the mitral valve (mitral click), which is determined immediately after the second sound with mitral stenosis. It is better heard in the patient's position on the left side and during exhalation in the form of a short high-frequency sound. The combination of the “clapping” 1st tone, 2nd tone and mitral click leads to the appearance of a specific three-part rhythm (“quail rhythm”), reminiscent of the phrase “time to sleep” - with an emphasis on the first word

In addition, during diastole, a rather loud tone can be heard, very similar to a mitral click - this is the so-called pericardial tone. It is heard in patients with constrictive pericarditis and, unlike the opening sound of the mitral valve, is not combined with the “popping” 1st sound.

In the middle or at the end of the systolic period, an additional sound may also be heard - a systolic click or “click”. It may be caused by sagging (prolapse) of the mitral valve leaflets (less commonly, tricuspid valve leaflets) into the atrium cavity or friction of the pericardial leaves in adhesive pericarditis.

The systolic click has a characteristic sound, a short and high-pitched tone, similar to the sound that occurs when the lid of a tin can bends.

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In clinical practice, the following changes in heart sounds are determined:

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

The most common reasons for weakening and increasing the volume of the main heart sounds are presented in table. 1.

Table 1.

. Splitting of the first heart sound. The main cause of splitting of the first heart sound is asynchronous closure and vibrations of the mitral and tricuspid valves. There are pathological and physiological splitting.

• Physiological splitting. In a healthy person, the mitral and tricuspid valves can also close asynchronously, which is accompanied by physiological splitting of the first sound.
• Pathological splitting. This situation can arise, for example, with blockade of the right bundle branch, which leads to a later than normal onset of contraction of the RV and, accordingly, to a later closure of the tricuspid valve.

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

Bifurcation and splitting of the second tone , as a rule, is associated with an increase in the duration of ejection of blood in the RV and/or a decrease in the time of ejection of blood in the LV, which leads, accordingly, to a later appearance of the pulmonary component and/or an earlier appearance of the aortic component of the second sound. There are pathological and physiological bifurcation and splitting of the second tone.

• Physiological splitting and bifurcation of the II tone. In healthy young people, inconsistent physiological splitting of the second tone may occur. It appears at the beginning of inspiration, when the blood flow to the right side of the heart and the filling of the vessels of the pulmonary circulation increases, which is accompanied by a slight increase in the duration of blood expulsion from the pancreas and a later appearance of the pulmonary component of the second tone. LV filling decreases during inspiration, as part of the blood is retained in the vessels of the pulmonary circulation. This leads to a slightly earlier appearance of the aortic component of the second sound.
• Pathological splitting and bifurcation of the II tone. In most cases, it is caused by an increase in the duration of blood expulsion from the pancreas with pronounced hypertrophy and decreased contractility. Pathological bifurcation and splitting of the second tone, in contrast to physiological splitting, is constant and persists during inhalation and exhalation.

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

In other cases, the appearance of a pathological III tone may only indicate increased rigidity 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 auscultation resembles a pronounced bifurcation of the first sound. In these cases, the three-part rhythm of the heart 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, in the diastolic form of CHF. The appearance of first degree AV block, as a rule, contributes to better detection of the pathological fourth tone.

Systolic gallop - a three-part rhythm that occurs when an additional short tone, or systolic click, appears during ventricular systole (between the first and second sounds). In most cases, the extra systolic click can be due to one of two reasons:

The impact of a portion of blood on the compacted wall of the ascending aorta at the very beginning of the period of expulsion of blood from the LV, for example, in patients with aortic atherosclerosis or hypertension (in these cases, a so-called early systolic click is recorded, auscultation resembling the splitting of the first sound;

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

Tone (click) of mitral valve opening appears exclusively with stenosis of the left AV orifice at the moment of opening of the mitral valve leaflets.

Normally, the valve flaps open silently. When the leaflets are fused in patients with mitral stenosis, at the moment of their opening, the initial portion of blood from the left atrium, under the influence of a high pressure gradient in the atrium and LV, hits the fused valve leaflets with great force, which leads to the appearance of a short click. It is better to listen to it at the apex of the heart or to the left of the sternum in the IV-V intercostal spaces; it is separated from the second sound by a short interval (phase of isovolumic relaxation of the ventricles).

The tone (click) of the opening of the mitral valve, together with the flapping I tone and the II tone accentuated on the pulmonary artery, form a peculiar melody of mitral stenosis, called the “quail rhythm” and reminiscent of certain quails (“sleep-in”).

A.V. Strutynsky
Complaints, anamnesis, physical examination