Characteristics of normal heart sounds. Auscultation of the heart: heart sounds What are heart sounds muffled rhythm correct

From early childhood, everyone is familiar with the actions of a doctor when examining a patient, when the heart rhythm is listened to using a phonendoscope. The doctor listens especially carefully to heart sounds, especially fearing complications after infectious diseases, as well as when complaining of pain in this area.

During normal heart function, the duration of the cycle at rest is about 9/10 of a second, and consists of two stages - the contraction phase (systole) and the rest phase (diastole).

During the relaxation stage, the pressure in the chamber changes less than in the vessels. Fluid under slight pressure is injected first into the atria and then into the ventricles. At the moment the latter are filled by 75%, the atria contract and force the remaining volume of fluid into the ventricles. At this time they talk about atrial systole. At the same time, the pressure in the ventricles increases, the valves slam shut and the areas of the atria and ventricles are isolated.

Blood presses on the muscles of the ventricles, stretching them, which causes a powerful contraction. This moment is called ventricular systole. After a split second, the pressure increases so much that the valves open and blood flows into the vascular bed, completely emptying the ventricles, in which a period of relaxation begins. At the same time, the pressure in the aorta is so high that the valves close and do not release blood.

The duration of diastole is longer than systole, so there is enough time for the heart muscle to rest.

Norm

The human hearing aid is very sensitive and picks up the most subtle sounds. This property helps doctors determine by the pitch of the sound how serious the disturbances in the heart are. Sounds during auscultation arise due to the work of the myocardium, valve movements, and blood flow. Heart sounds normally sound sequential and rhythmic.

There are four main heart sounds:

occurs when a muscle contracts. It is created by vibration of the tense myocardium, noise from the operation of the valves. It is heard in the area of the apex of the heart, near the 4th left intercostal space, and occurs synchronously with the pulsation of the carotid artery.
occurs almost immediately after the first. It is created due to the slamming of valve flaps. It is more deaf than the first and can be heard on both sides in the second hypochondrium. The pause after the second sound is longer and coincides with diastole.
optional tone, normally its absence is allowed. It is created by vibration of the walls of the ventricles at the moment when there is additional blood flow. To determine this tone you need sufficient listening experience and absolute silence. It can be heard well in children and adults with a thin chest wall. It is more difficult for obese people to hear it.
another optional heart sound, the absence of which is not considered a violation. Occurs when the ventricles fill with blood during atrial systole. Sounds great in thin people and children.

Pathology

Sound disturbances that occur during the work of the heart muscle can be caused by various reasons, grouped into two main ones:

Physiological, when changes are associated with certain characteristics of the patient’s health. For example, fat deposits in the listening area impair the sound, so heart sounds are muffled.
Pathological when changes affect various elements of the cardiac system. For example, increased density of the atrioventricular orifice valves adds a click to the first tone and the sound is louder than usual.

Pathologies that arise during work are primarily diagnosed by auscultation by a doctor during examination of the patient. The nature of the sounds is used to judge a particular violation. After listening, the doctor must record a description of the heart sounds in the patient’s chart.

Heart sounds that have lost the clarity of their rhythm are considered muffled. When dull tones weaken in the area of all auscultation points, it leads to the assumption of the following pathological conditions:

serious myocardial damage - extensive, inflammation of the heart muscle, proliferation of connective scar tissue;
exudative pericarditis;
disorders not related to cardiac pathologies, for example, emphysema, pneumothorax.

If only one tone is weak at any listening location, the pathological processes leading to this are called more precisely:

voiceless first tone, heard at the apex of the heart indicates inflammation of the heart muscle, its sclerosis, partial destruction;
dull second tone in the area of the second intercostal space on the right speaks of or narrowing of the aortic mouth;
dull second tone in the area of the second intercostal space on the left indicates pulmonary valve insufficiency.

There are such changes in the tone of the heart that experts give them unique names. For example, “quail rhythm” - the first clapping tone is replaced by the second normal one, and then the echo of the first tone is added. Severe myocardial diseases are expressed in a three-member or four-member “gallop rhythm,” that is, blood fills the ventricles, stretching the walls, and vibration vibrations create additional sounds.

Simultaneous changes in all tones at different points are often heard in children due to the structure of their chest and the close location of the heart to it. The same can be observed in some adults of the asthenic type.

Typical disturbances can be heard:

high first sound at the top of the heart appears when the left atrioventricular opening is narrow, as well as when;
high second tone in the second intercostal space on the left indicates increasing pressure in the pulmonary circulation, which causes strong flapping of the valve leaflets;
high second tone in the second intercostal space on the right shows an increase in pressure in the aorta.

Interruptions in heart rhythm indicate pathological conditions of the system as a whole. Not all electrical signals travel equally through the thickness of the myocardium, so the intervals between heartbeats are of different durations. When the atria and ventricles work uncoordinated, a “cannon tone” is heard - the simultaneous contraction of the four chambers of the heart.

In some cases, auscultation of the heart shows a separation of the tone, that is, the replacement of a long sound with a pair of short ones. This is due to a violation of the coordination of the muscles and valves of the heart.

The separation of the 1st heart sound occurs for the following reasons:

closure of the tricuspid and mitral valves occurs in a temporary gap;
contraction of the atria and ventricles occurs at different times and leads to disruption of the electrical conductivity of the heart muscle.
The separation of the 2nd heart sound occurs due to the difference in the time of slamming of the valve leaflets.

This condition indicates the following pathologies:

excessive increase in pressure in the pulmonary circulation;
proliferation of left ventricular tissue with mitral valve stenosis.

With cardiac ischemia, the tone changes depending on the stage of the disease. The onset of the disease is poorly expressed in sound disturbances. During the periods between attacks, no deviations from the norm are observed. The attack is accompanied by a frequent rhythm, indicating that the disease is progressing, and heart sounds in children and adults change.

Medical professionals pay attention to the fact that changes in heart sounds do not always indicate cardiovascular disorders. It happens that the causes are a number of diseases of other organ systems. Muted tones and the presence of additional tones indicate diseases such as endocrine diseases and diphtheria. An increase in body temperature is often expressed in a disturbance in heart tone.

A competent doctor always tries to collect a complete medical history when diagnosing a disease. In addition to listening to heart sounds, he interviews the patient, carefully reviews his chart, and prescribes additional examinations according to the expected diagnosis.

Auscultation of the heart is usually carried out sequentially: in a supine (on the back), in a standing position of the patient, and also after physical activity (gymnastics). To ensure that respiratory sounds do not interfere with listening to sounds of cardiac origin, before listening, it is necessary to ask the patient to inhale, exhale completely and then hold his breath in the exhalation position. This technique is especially important for beginners in the study of auscultation.

Auscultation of the heart is preferably done indirectly, with a stethoscope. Due to the fact that individual places for listening to the heart are located at a very close distance from each other, direct auscultation with the ear is used in exceptional cases to complement the mediocre one. To correctly assess auscultation data, you need to know the places of projection of the heart valves on the chest wall and the best places to listen to them, since sound vibrations depend not only on the proximity of the valve apparatus, but also on the conduction of these vibrations along the blood flow.

Projection of valves on the chest:
1. The valve of the pulmonary trunk lies behind the cartilage of the third left rib near the sternum and partly behind it;
2. The aortic valve lies behind the sternum immediately below and deeper than the opening of the pulmonary trunk;
3. The mitral valve is projected at the site of attachment to the sternum of the cartilage of the fourth left rib;
4. The tricuspid valve lies behind the sternum almost in the middle between the places of attachment of the cartilages of the V right and III left ribs.
In healthy people, during auscultation of the heart, two tones can be clearly heard: the first sound, which occurs during systole, is systolic, and the second sound, which occurs during diastole, is diastolic.

Beginning clinicians need to accustom themselves to systematically paying attention to all the features of sound phenomena and pauses. The first task is the orienting determination of the first tone, since the sound cycle of the heartbeat begins with it. Then all four openings of the heart are heard in sequential order.

Listening places:
The most distinct tone of the mitral valve is heard at the apex of the heart (1.5 - 2.0 cm medially from the left midclavicular line), the pulmonary valve - in the second left intercostal space at the edge of the sternum, the tone of the aorta - at the edge of the sternum in the second right intercostal space, tricuspid valve - at the base of the xiphoid process of the sternum; the aortic valve is also heard at the attachment site of the III-IV ribs - Botkin-Erb point (V point of auscultation). Listening to the valves is carried out in the specified sequence, corresponding to a decrease in the frequency of their damage.
For each subject it is necessary to determine:
1. strength or clarity of tones;

2. timbre of tones;

3. frequency,

5. presence or absence of noise.

When listening to a healthy heart, two tones are heard, periodically replacing each other. Starting auscultation of the heart from the apex, we hear:

1. short, stronger sound - first tone,

2. short first pause,

3. weaker and even shorter sound - second tone

4. a second pause, twice as long as the first.

The first tone, in contrast to the second, is somewhat longer, lower in tone, stronger at the apex, weaker at the base, and coincides with the apical impulse. It is more convenient for beginners to distinguish the first tone from the second, focusing on a short pause, that is, guided by the fact that the first tone is heard before it, or, in other words, a short pause follows the first tone. In the case of a frequent heart rhythm, when it is not possible to clearly differentiate the tones, you need to place the fingers of your right hand at the site of the apical impulse (or to the carotid artery in the neck) while listening. The tone that matches the impulse (or the carotid pulse) will be the first. It is impossible to determine the first heart sound by the pulse on the radial artery, since the latter is delayed in relation to the first heart sound.

First tone is formed from 4 main components:

1. Atrial component- associated with vibrations of the atrial myocardium. Atrial systole precedes ventricular systole, so normally this component merges with the first sound, forming its initial phase.

2. Valve component- oscillation of the atrioventricular valve leaflets in the contraction phase. The magnitude of the oscillations of the leaflets of these valves is influenced by intraventricular pressure, which in turn depends on the speed of contraction of the ventricles.

3. Muscle component - also occurs during the period of ventricular contraction and is caused by myocardial fluctuations.

4. Vascular component- formed due to vibrations of the initial parts of the aorta and pulmonary trunk during the period of expulsion of blood from the heart.

Second tone occurring at the beginning of diastole, is formed by 2 main components:
1. Valve component- slamming of the aortic and pulmonary valves.
2. Vascular component- vibration of the walls of the aorta and pulmonary trunk.

Third tone is caused by fluctuations that appear during rapid relaxation of the ventricles, under the influence of the flow of blood flowing from the atria. This tone can be heard in healthy people, mainly in young people and adolescents. It is perceived as a weak, low and dull sound at the beginning of diastole, 0.12-0.15 s from the beginning of the second tone.

Fourth tone precedes the first sound and depends on the oscillations that occur during atrial contraction. For children and adolescents it is considered physiological; its appearance in adults is pathological.

The third and fourth sounds are better heard during direct auscultation and are clearly identified when recording a phonocardiogram. The detection of these tones in elderly people, as a rule, indicates severe myocardial damage.

Changes in heart sounds

Muting both tones observed with a decrease in the contractility of the heart muscle, may be under the influence of extracardiac causes (excessive subcutaneous fat, anasarca, significant development of the mammary glands in women, pronounced development of the chest muscles, pulmonary emphysema, accumulation of fluid in the cavity of the heart sac: and also as a result damage to the heart itself (myocarditis, cardiosclerosis, due to decompensation in various heart diseases).

Boosting both tones heart disease depends on a number of extracardiac causes (thin chest, retraction of the pulmonary edges, tumors of the posterior mediastinum) and can be observed with thyrotoxicoea, fever and some intoxications, for example, caffeine.

More often, a change in one of the tones is observed, which is especially important in the diagnosis of heart disease.

Weakening of the first tone at the apex of the heart is observed with mitral and aortic valve insufficiency (due to the absence of a period of closed valves during systole), with narrowing of the aortic mouth and with diffuse myocardial lesions (due to dystrophy, cardiosclerosis, myocarditis) with myocardial infarction.

With insufficiency of the tricuspid valve and the pulmonary valve, weakening of the first tone is observed at the base of the xiphoid process due to weakening of the muscular and valvular components of these valves. A weakened first sound in the aorta is one of the characteristic acoustic signs of aortic semilunar valve insufficiency. This occurs due to an increase in intraventricular pressure above the level of the left atrial pressure at the end of diastole, which promotes earlier closure of the mitral valve and limits the amplitude of movement of its leaflets.

Strengthening the first tone(popping sound) at the apex of the heart is observed when the filling of the left ventricle with blood decreases during diastole and is one of the characteristic signs of stenosis of the left atrioventricular orifice. The reason for its intensification is the compaction of the mitral valve leaflets due to their fibrous changes. These structural features of the valve determine the change in the frequency-amplitude characteristics of the first tone. Dense tissues are known to generate higher frequency sounds. The first tone (“Strazhesko’s cannon tone”) is especially loud during complete atrioventricular heart block, when simultaneous contraction of the atria and ventricles occurs. An increase in the first tone at the base of the xiphoid process is observed with stenosis of the right atrioventricular orifice; it can also be observed with tachycardia and extrasystole.

Weakening of the second tone above the aortic valve is observed when it is insufficient, either due to partial or complete destruction of the aortic valve leaflets (in the second case, the second sound may be completely absent), or due to their cicatricial compaction. Weakening of the second tone in the pulmonary artery is observed when its valve is insufficient (which is extremely rare) and when pressure in the pulmonary circulation decreases.

Strengthening the second tone on the aorta is observed with increased pressure in the systemic circulation in diseases accompanied by arterial hypertension (hypertension, glomerulonephritis, polycystic kidney disease, etc.). A sharply enhanced second tone (clangor) is observed in syphilitic mesaortitis. An increase in the second tone in the pulmonary artery is observed with an increase in pressure in the pulmonary circulation (mitral heart defects), difficulty in blood circulation in the lungs (pulmonary emphysema, pneumosclerosis). If this tone is louder above the aorta, they speak of the accent of the second tone on the aorta, but if it is louder above the pulmonary trunk, they speak of the accent of the second tone on the pulmonary artery.

Split heart sounds.

Heart sounds, components T several components are perceived as a single sound. In some physiological and pathological conditions, the sound of those components that take part in the formation of a particular tone does not synchronize. There is a split tone.

Split tones is the separation of the components that make up the tone. The latter follow each other at a short interval (every 0.036 s or more). The mechanism of bifurcation of tones is due to asynchronism in the activity of the right and left half of the heart: non-simultaneous closure of the atrioventricular valves leads to bifurcation of the first tone, of the semilunar valves - to bifurcation of the second tone. Split tones can be physiological and pathological. Physiological splitting (splitting) of the first tone occurs when the atrioventricular valves close asynchronously. This can happen during deep exhalation, when, due to increased pressure in the pulmonary circulation, blood enters the left atrium with greater force and prevents the timely closure of the mitral valve.

Physiological splitting of the second tone manifests itself in connection with different phases of breathing, since during inhalation and exhalation the blood supply of the left and right ventricles changes, and, consequently, the duration of their systole and the time of closure of the corresponding valves. The bifurcation of the second tone is especially well detected during auscultation of the pulmonary artery. The physiological bifurcation of the second tone is not constant (unfixed bifurcation), is closely related to the normal breathing mechanism (during inspiration it decreases or disappears), while the interval between the aortic and pulmonary components is 0.04-O. Obs.

Pathological split tones may be due to the following factors:

1. Hemodynamic (increase in the systolic volume of one of the ventricles, increase in diastolic pressure in one of the ventricles, increase in diastolic pressure in one of the vessels);

2. Violation of intraventricular conduction (bundle branch block);

3. Weakening of the contractile function of the myocardium;

4. Ventricular extrasystole.

Pathological splitting of the first tone may be due to disruption of intraventricular conduction (along the bundle branches) due to a delay in the next contraction of one of the ventricles.

Pathological bifurcation II tone is observed with arterial hypertension, with stenosis of the aortic mouth, when the leaflets of the aortic valve slam shut later than the pulmonary valve; in case of increased pressure in the pulmonary circulation (with emphysema, mitral stenosis, etc.), when, on the contrary, the pulmonary valve lags behind.

One should distinguish from split tones the appearance additional tones.

These include mitral valve opening tone, heard when the left atrioventricular orifice narrows. The mechanism of its occurrence is associated with a sudden tension of the sclerotic valve leaflets, unable to move completely to the walls of the ventricle as blood passes from the left atrium to the left ventricle. The opening tone of the mitral valve occurs immediately after the second tone, after 0.07-0.1 sec, during diastole. It is best heard at the apex and is combined with other auscultatory signs of mitral stenosis. In general, the additional third sound of the mitral valve opening in combination with a loud (clapping) first sound and second heart sound form a three-part rhythm, reminiscent of the cry of a quail, - quail rhythm.

The three-part rhythm also includes rhythm gallop, reminiscent of the tramp of a galloping horse. There is a presystolic gallop rhythm, which is caused by a pathological IV heart sound, and a summation gallop rhythm, the occurrence of which is associated with the overlap of the III and IV sounds; an additional tone with this rhythm is usually heard in mid-diastole. A gallop rhythm is heard in case of severe myocardial damage (myocardial infarction, myocarditis, chronic nephritis, hypertension, etc.).

With severe tachycardia, a shortening of the diastolic pause to the size of the systolic pause is observed. At the apex, tones I and II become almost identical in sonority, which served as the basis for calling such an auscultatory picture pendulum-like rhythm or, similar to the fetal heartbeat, embryocardia. This can be observed in acute heart failure, paroxysmal tachycardia, high fever, etc.

Heart murmurs

Murmurs can occur both inside the heart itself (intracardial) and outside it (extracardiac).

The main mechanisms for the formation of intracardiac murmurs are changes in the size of the orifices of the heart and changes in the speed of blood flow. Their occurrence may depend on the rheological properties of the blood, and sometimes on the irregularities of the endocardium of the valves, as well as the condition of the intima of the vessels.

Intracardiac murmurs are divided into organic, which are caused by anatomical changes in the orifices and valve apparatus (acquired and congenital defects) and inorganic or functional, occurring with anatomically intact valves and associated with changes in the activity of the heart, with a decrease in blood viscosity

An intermediate position between organic and functional noises is occupied by the noise of relative muscular insufficiency of the valves. Relative valve incompetence noise occurs when the ventricles dilate, and, consequently, the atrioventricular opening expands, and therefore even an unchanged valve cannot completely close it. As myocardial contractility improves, the noise may disappear. A similar mechanism occurs when the tone of the papillary muscles is disturbed.

Based on the time of noise appearance in relation to the phases of cardiac activity, systolic and diastolic cardiac murmurs are distinguished.

Systolic murmurs are heard between the I and D sounds (during a short pause), and diastolic murmurs are heard between the P and the next I tone (during a long pause). Noise may occupy the entire pause or only part of it. Based on their hemodynamic origin, ejection sounds and regurgitation sounds are distinguished.

Systolic murmurs can be organic and functional; their intensity is usually stronger than diastolic ones.

Systolic murmur occurs when blood encounters an obstacle on its way. It is divided into two main types:

1. Systolic ejection murmur(with stenosis of the aortic mouth or pulmonary trunk: since during the expulsion of blood from the ventricles, a narrowing of the vessel occurs along the path of the blood flow);

2. Systolic regurgitation murmur(with insufficiency of the mitral or tricuspid valves; in these cases, during ventricular systole, blood flows not only into the aorta and pulmonary trunk, but also back into the atria through an incompletely covered atrioventricular orifice.) Diastolic murmur occurs either with stenosis of the atrioventricular orifices, since during diastole, there is a narrowing in the path of blood flow from the atria to the ventricles, or in case of insufficiency of the aortic valve or pulmonary valve - due to the reverse flow of blood from the vessels into the ventricles in the diastole phase.

Based on their properties, noises are distinguished:

1. by timbre (soft, blowing; or rough, scraping, sawing);

2. by duration (short and long),

3. by volume (quiet and loud);

4. by intensity in dynamics (decreasing or increasing noise);

PLACES OF BEST LISTENING AND NOISE CONDUCTION:

Murmurs are heard not only in the classic places where sounds are heard, but also at some distance from them, especially along the path of the blood flow. For stenosis of the aortic mouth the noise is carried out in the carotid and other large arteries and is even heard on the back at the level of the I - III thoracic vertebrae. Murmur of aortic valve insufficiency carried out, on the contrary, to the ventricle, i.e. to the left and down, and the place of listening passes along this line to the sternum, to its left edge, at the place of attachment of the third costal cartilage. In the initial stages of damage to the aortic valves, for example with rheumatic endocarditis, a gentle diastolic murmur, as a rule, is not heard at the usual place (second intercostal space on the right), but only at the left edge of the sternum in the third or fourth intercostal space - at the so-called fifth point. Noise due to bicuspid valve insufficiency is carried up to the second intercostal space or to the left to the armpit. In case of insufficiency of the interventricular septum the noise spreads across the sternum from left to right.

All noise during conduction loses strength in proportion to the square of the distance; this circumstance helps to understand their localization. In the presence of mitral valve insufficiency and aortic stenosis, we, going from the apex along the line connecting the places where they are heard, will first hear the decreasing noise of moral insufficiency, and then the increasing noise of aortic stenosis. Only presystolic murmur with mitral stenosis has a very small range of distribution; sometimes it is heard in a very limited area.

Systolic murmurs of aortic origin (narrowing of the orifice, unevenness of the aortic wall, etc.) are well heard in the suprasternal fossa. With significant expansion of the left atrium, the systolic murmur of mitral insufficiency is sometimes heard to the left of the spine at the level of the VI - VII thoracic vertebrae.

Diastolic murmurs ,

depending on what part of the diastodes occur, they are divided into protodiastolic (at the beginning of diastole, Greek protos - first), mesodiastolic (occupying only the middle of diastole, Greek mesos - middle) and presystolic or telediastolic (at the end of diastole, increasing to first tone noise, Greek telos - end). The vast majority of diastolic murmurs are organic. Only in some cases can they be heard without the presence of organic damage to the valves and orifices.

Functional diastolic murmurs.

There are functional presystolic Flint noise, when in case of aortic valve insufficiency, a reverse wave of blood lifts the cusp of the moral valve, narrowing the left atrioventricular orifice, thereby creating relative mitral stenosis. Mesodiastolic Coombs noise may occur at the beginning of an attack of rheumatism due to swelling of the left atrioventricular orifice and the occurrence of its relative stenosis. When the exudative phase is removed, the noise may disappear. Graham-Still noise can be determined in diastole above the pulmonary artery, when congestion in the pulmonary artery causes stretching and expansion of the pulmonary artery, resulting in relative insufficiency of its valve.

If there is noise, it is necessary to determine its relationship to the phases of cardiac activity (systolic or diastolic), to clarify the place of its best listening (epicenter), conductivity, strength, variability and character.

Characteristics of murmurs in some heart defects.

Mitral valve insufficiency is characterized by the presence of a systolic murmur at the apex of the heart, which is heard together with a weakened first sound or instead of it, decreases towards the end of systole, is quite sharp, rough in nature, is well carried into the armpit, and is better heard with the patient positioned on the left side.

At stenosis of the left atrioventricular orifice The noise occurs in the mesodiastole, has an increasing character (crescendo), is heard at the apex, and is not carried anywhere. Often ends with a clapping 1st tone. It is better determined with the patient positioned on the left side. Presystolic murmur, clapping 1st tone and “double” 2nd tone give a typical melody of mitral stenosis.

At aortic valve insufficiency diastolic murmur begins immediately after the 2nd sound, in protodiastole, gradually decreasing towards its end (decrescendo), better heard at the 5th point, weaker detected in the 2nd intercostal space to the right of the sternum, carried out at the apex of the heart, the murmur is soft, better heard during breath-holding after take a deep breath. It is better heard when the patient is standing, especially when the torso is tilted forward.

In cases aortic stenosis a systolic murmur is heard in the second intercostal space on the right at the edge of the sternum. It is very sharp, rough, drowns out the first sound, is heard throughout the entire systole and has the greatest conductivity, is well heard on the vessels of the neck, on the back along the spine.

At tricuspid valve insufficiency The maximum sound of the noise is determined at the base of the xiphoid process of the sternum. With organic damage to the valve, the systolic murmur is rough and clear, and with relative valve insufficiency it is softer and blowing.

Of the rarer defects in which systolic murmur is determined, they indicate pulmonary stenosis(its maximum sound is in the second intercostal space to the left of the sternum, extends to the left clavicle and to the left half of the neck); patent ductus Botallova(systole-diastolic murmur in the 3rd-4th intercostal spaces); ventricular septal defect(in the 4th intercostal space, slightly outward from the left edge of the sternum, it is carried out in the form of “spokes of a wheel” - from the epicenter of the noise in a circle, loud, sharp in timbre).

Extracardiac (extracardiac) murmurs.

Murmurs can occur not only inside the heart, but also outside it, synchronously with heart contractions. There are pericardial murmurs or pericardial friction murmurs and pleuropericardial friction murmurs.

Pericardial murmur heard mainly due to inflammatory phenomena in the pericardium, with myocardial infarction, with tuberculosis with fibrin deposition, etc. Pericardial friction noise is characterized by:

1. It is either barely noticeable or very rough, and upon direct auscultation sometimes even causes unpleasant sensations, since it is heard directly under the ear,

2. The murmur is associated with the phases of cardiac activity, but not exactly: it moves from systole to diastole and back (it is usually stronger in systole);

3. Almost never radiates,

4. Variable in location and time;

5. When bending forward, when standing on all fours, and when pressing with a stethoscope, the noise intensifies.

Along with pericardial murmur, a false pericardial (pleuropericardial) friction murmur is distinguished, associated with dry pleurisy of the parts of the pleura adjacent to the heart, mainly on the left. Contractions of the heart, increasing the contact of the pericardium and pleura, contribute to the appearance of a friction noise. The difference from true pericardial murmur is that it is heard only during deep breathing, intensifies during inspiration, and is localized predominantly at the left edge of the heart.

Cardiopulmonary murmurs arise in the parts of the lungs adjacent to the heart, which expand during systole due to a decrease in the volume of the heart. Air, penetrating into this part of the lungs, produces a noise that is vesicular in nature (“vesicular breathing”) and systolic in time.

Auscultation of arteries and veins.

In a healthy person, you can listen to tones in medium-sized arteries (carotid, subclavian, femoral, etc.). Like the heart, two tones are often heard on them. The arteries are first palpated, then the stethoscope funnel is applied, trying not to compress the vessel, avoiding the occurrence of stenotic noise.

Normally, two sounds are heard (systolic and diastolic) on the carotid and subclavian arteries. On the femoral artery, only the first, systolic sound can be heard. In both cases, the first tone is partially conductive and partially formed at the site of auscultation. The second sound is carried out entirely from the semilunar valves.

The carotid artery is heard at the level of the larynx on the inside of the m. Stemo-cleido-mastoidei, and the subclavian - on its outer side, immediately above the collarbone or under the collarbone in its outer third. Listening to other arteries does not produce any sounds.

In case of aortic valve insufficiency with a pronounced rapid pulse (pulsus celer), sounds can also be heard above arteries where they are usually not heard - above the abdominal aorta, brachial, radial arteries. With this defect, two tones are sometimes heard above the femoral artery ( Traube double tone), due to sharp fluctuations of the vascular wall both in the systole and diastole phases. In addition, sounds in the peripheral arteries can occur with pronounced hypertrophy of the left ventricle and with thyrotoxicosis due to increased pulsation of blood vessels.

Murmurs may also be heard above the arteries. This is observed in the following cases:

1. Conducted through the blood flow for stenosis of the aortic mouth, atherosclerosis with intimal changes and aneurysms;

2. Systolic, associated with a decrease in blood viscosity and an increase in blood flow speed (with anemia, fever, thyrotoxicosis;

3. Local - when the artery is compressed from the outside (for example, by pleural cords around the subclavian artery), its sclerotic stenosis, or, conversely, when it has an aneurysm;

4. in case of aortic valve insufficiency on the femoral artery, with slight compression, it is heard double Vinogradov-Durozier noise, in the first phase caused by compression of the stethoscope, in the second, probably by reverse blood flow.

When listening to the veins, they use exclusively auscultation of the bulb of the jugular vein above the collarbone, usually on the right. The stethoscope must be placed very carefully to avoid noise from compression. With a decrease in blood viscosity, due to an increase in blood flow in patients with anemia, a noise is heard here, continuously, almost regardless of heart contractions. It is musical and low in character and is called "spinning top noise". This noise is better heard when turning the head in the opposite direction. This noise does not have any particular diagnostic significance, especially since it can rarely be observed in healthy people.

In conclusion, it should be noted that in order to hear the heart, you need to learn to listen to it. First, it is necessary to repeatedly listen to healthy people with a slow heart rate, then with tachycardia, then with atrial fibrillation, setting the task of distinguishing tones. Gradually, as experience is gained, the analytical method of studying the melody of the heart must be replaced by a synthetic one, when the entire set of sound symptoms of this or that. of another defect is perceived as a whole, which speeds up the diagnostic process. However, in difficult cases, one should try to combine these two approaches to the study of acoustic phenomena of the heart. For novice doctors, a detailed verbal description of the melody of each patient’s heart, performed in a certain sequence that repeats the sequence of auscultation, is considered very useful. The description should include characteristics of heart sounds at all listening points, as well as the main properties of the noise. It is advisable to use the graphic image of the heart melody used in clinics. Both of these methods are aimed at developing the habit of systematic auscultation.

Self-training in auscultation must be pursued persistently, without being upset by the inevitable failures at first. It should be remembered that “the learning period for auscultation lasts a lifetime.”

As the heart operates, a pressure difference (pressure gradient) periodically occurs in its chambers and great vessels, which contributes to the opening and closing of the heart valves. The work of the valves, the tension of the muscle structures and great vessels during the period of expulsion of blood from the ventricles create corresponding vibrations, which we perceive auscultatively as tones (Fig. 331). In essence, these are not tones, but noises - aperiodic, multi-part vibrations. But in domestic medicine they are usually called tones. For practical purposes, this is convenient, since there is no confusion between heart sounds and murmurs that occur with heart defects.
The opening of the heart valves is accompanied by the appearance of low-frequency vibrations, which our ear does not perceive, but when

When the valves close, high-frequency oscillations always occur, which we listen to in the form of heart sounds.
The tones that arise are clearly associated with the phases of cardiac activity - with systole and diastole of the ventricles.
Ventricular systole has several phases (Fig. 332):

blood vessels leads to the opening of the semilunar valves of the aorta and pulmonary artery;

ejection phase - begins immediately after the opening of the aortic and pulmonary artery valves, the force of contraction of the ventricles increases towards the end of the ejection phase, blood is expelled from the ventricles into the great vessels.

Ventricular diastole begins after the end of the ejection period with a phase of isometric (isovolumic) relaxation of the ventricles, during which the pressure in the ventricles drops, the resulting gradient between low pressure in the ventricles and high pressure in the great vessels provokes a reverse flow of blood from the vessels into the ventricles, which closes the semilunar valves of the aorta and pulmonary artery.
The decrease in ventricular pressure causes the mitral and tricuspid valves to silently open. This is facilitated by
pressure gradient between the atria and ventricles (in the atria it is 5-10 mm Hg, in the ventricles 0-5 mm Hg) Due to the pressure difference, gradual filling of the ventricles occurs, at first quickly - a phase of rapid filling of the ventricles then slow - slow filling phase or diastasis. At a normal heart rate, diastasis occupies most of the diastole. After diastasis, a phase of active filling of the ventricles begins due to contraction of the atria - a period of rapid active diastolic filling of the ventricles. At the end of this phase, the leaflet valves float up.
Then the cycle repeats.
In clinical practice, both phases of cardiac activity - tolu and diastole - are usually divided into certain segments or periods. This is necessary to understand the origin and differentiation of additional heart sounds and murmurs.
Foreign clinicians divide systole into 3 parts - protosystole (the initial part of systole), mesosystole - the middle part, and telesystole - the final part (Tsukerman, 1963). In our country, this division is almost never used; systole is divided into physical segments - a third, half or all of the systole.
There are 3 periods in diastole (Fig. 333). The division is based on taking into account some landmarks on the ECG, PCG and sphygmogram recorded synchronously:

Rice. 333. Synchronous recording of ECG and FCG. Phase of cardiac activity systole and diastole, reference points for their reference, division of diastole into 3 periods

protodiastole, it corresponds to the segment from II to III tone (III tone occurs 0.12-0.19 s from the beginning of the tone); Without

tone, the end of protodiastole can be a point located in the middle of the distance between the second tone and the beginning of presystole; protodiastole includes a period of isometric relaxation of the ventricles and their rapid passive filling;

mesodiastole, it lies between protodiastole and presystole, which approximately corresponds to the phase of slow filling of the ventricles;
presystole, the final part of diastole, it is determined from the beginning of the P wave on the ECG to the Q wave and corresponds to the period of rapid active filling of the ventricles as a result of contraction (systole) of the atria.

Clinical characteristics of tones
When auscultating the heart, 2 tones are heard at the apex and base of the xiphoid process, with emphasis on the first (Fig. 334).
/ systole diastole / systole diastole
Tam ta Tam ta
I tone II tone I tone II tone
The tones are separated by silent periods:

systole (systolic pause) silent expulsion of blood from the ventricles;
diastole (diastolic pause) silent filling of the ventricles. The first silent period is short, the second is 1/3-1/2 longer than the first. The difference in the duration of systole and diastole depends on the heart rate; the more often the heart contracts, the smaller the difference between them.

The first, louder syllable (Tam) corresponds to the I tone. The first sound occurs at the beginning of ventricular systole after a long pause. That is why it is called systolic. Its duration is 0.09-0.12 s, it is of low timbre, louder at the apex than at the sternum near the xiphoid process, which is due to the greater systolic tension of the left ventricle and the more superficial location of the apex. At the base of the xiphoid process, the first tone is less loud than at the apex.

I TONE II tone

Base

Top
Base - -
Rice. 334. Phonocardiogram and diagram of normal tones when listening to the apex and base of the heart
The height of the oscillations and bars is reflective! sonority (loudness) tygt; and A short pause is systole, a long pause is diastole.
When listening to the heart at the base in the second intercostal space on the right and left at the edge of the sternum, after a short auscultatory pause (ventricular systole), 2 tones are also heard, but with emphasis on the second syllable, more loudly.
systole / diastole systole / diastole
there Ta there Ta
I tone II tone I tone II tone
The sounding second syllable corresponds to tone II. The second tone arose at the beginning of diastole, therefore it is called a diastolic tone (gt; and shorter (0.05-0.07 s) than the first tone, higher.
On auscultation, the sound of the second sound in the aorta and pulmonary artery is the same, although the pressure in the pulmonary artery is significantly lower than in the aorta. The similarity of sound is explained by the fact that the valves of the pulmonary artery lie more superficially, closer to the chest wall, while the valves of the aorta are more distant from it.

The mechanism of occurrence of I and I, III and IV tones
In the occurrence of the first tone, the leading role belongs to three factors:

vibrations of the tense leaflets of the mitral and tricuspid valves at the beginning of systole in the phase of isometric tension of the ventricles, when all valves are closed;
vibrations of the muscles of the ventricles, septum, papillary muscles, chords during isometric stress;
fluctuations in the initial sections of the aorta and pulmonary artery at the beginning of the period of expulsion of blood from the ventricles.

The second sound is formed at the beginning of diastole by the closure of the aortic and pulmonary artery valves by the reverse flow of blood from the vessels into the ventricles, which are in a state of relaxation. A minor role in the occurrence of the second sound belongs to the vibration of the walls of the aorta and pulmonary artery, caused by the same reverse flow of blood. The third sound. Physiological III tone is heard in children, adolescents and young people of asthenic physique. Its appearance in another category of patients, middle-aged people, and even more so in older age groups, indicates the need for in-depth cardiac examination. The third tone is heard shortly (0.12-0.15 s) after the second sound. It is located in protodiastole and is perceived as an echo of the second tone (Fig. 335).

Rice. 335. Third physiological tone.

The third sound occurs due to vibrations of the walls of the ventricles during their rapid passive filling with blood at the beginning of diastole. The main condition for the appearance of the third tone is high tone and elasticity of the myocardium, which is present in children and young people.
The third tone has a low timbre, it is quiet and short (0.03-0.06 s). The third sound is heard at the apex of the heart and above the zone of absolute cardiac dullness, preferably with the patient lying on his back, but more often within 1-3 minutes after moving from a vertical to a horizontal position. Sometimes it can be heard when the patient is lying down during a deep exhalation or in a position on the left side. In a vertical position, the third sound is heard extremely rarely.
Fourth tone. The physiological fourth tone is also heard in adolescents and young adults, but very rarely. It occurs following contraction of the atria at the moment of rapid filling of the ventricles and is associated with vibration of the walls of the ventricles, which have high tone and good elasticity. The IV tone is best heard while lying down, while exhaling. The place of listening is the apex.

the tone is perceived as a short (0.03-0.10 s), quiet sound immediately before the first tone, that is, at the end of diastole, the melody of the heart sounds like this (Fig. 336):

(ta) /

Rice. 336. Fourth physiological tone.

On the phonocardiogram, the IV tone has 2-3 low-amplitude ascillations, occurring 0.08-0.15 s from the beginning of the P wave on the ECG.
The main features of I, II, 111, IV tones are briefly presented in table. 10.
Table 10. Main signs of normal heart sounds

Signs	1 1011	II junior	Ill be young	IV tone
Best listening places	Top	Base	Top or closer to 1 ore	Top
Relation to cardiac phases	Vo shushes at the beginning of systole after a large ausculatory paucity after diastole	In *none at the beginning of diastole after small ausculatory pauiigt;1 - after systole	Occurs at the beginning of diastole shortly after the second sound	Occurs at the end of diastole before the first sound
Continuous ib	0.09 0.12 s	0.05 0.07 s	0.03 -0.06 s	0.03-0.10 s
The hour is more typical	30-120 Hz	70-150 Hz	10 70 Hz	70-100 Hz
Ausculative characteristics	Loud, low, long lasting, louder at the top	Loud, high, short, louder at the base		Quiet, deaf, low, short
Coincidence with the apex beat	Matches	11th matching	Does not match	Does not match

The most important element of a qualified auscultation of the heart is the ability to distinguish the first tone from the second (Table 10), correctly determine the phases of cardiac activity - systole and diastole, and correctly correlate additional sounds and noises to the phases of cardiac activity. All this is the basis for the clinical diagnosis of a healthy or diseased heart. If it is difficult to distinguish between sounds I and II by auscultation, then the technique of simultaneous auscultation of the heart and palpation of the apex beat is used. To do this, the phonendoscope must be shifted from the apex towards the sternum, and

Place the top with 2 fingers of the right hand. The tone coinciding with the apex beat is the first tone. In the case when the apical impulse is not palpable, they focus on the pulsation of the carotid artery. The phonendoscope is installed at the apex of the heart, and 2 fingers of the right hand are placed on the carotid artery in the carotid triangle, but without pinching it. Normally, the pulsation of the carotid artery almost coincides with the first sound, lagging only 0.1 s. Focusing on the pulsation of the radial artery is less reliable, since this delay increases to 0.15-0.24 s.
So, to distinguish between I and II tones, you need to focus on:

place of listening: I tone is heard and characterized by qualities at the apex, II sound - at the base of the heart,
the relationship of tones to auscultatory pauses, that is, to the phases of cardiac activity: I follows a long auscultatory pause (diastole), II follows a short one (systole);
volume: I tone is louder at the apex, II tone - at the base of the heart;
pitch of the tones: I tone is more low, dull, II tone is higher, sonorous;
duration: I tone is longer, II tone is shorter;
coincidence with the apex beat: the 1st tone coincides with the apex beat, the 2nd tone does not coincide, it sounds at the moment of the absence of the apex beat and the carotid artery pulse.

With a high heart rate (emotional, physical shock), it is often difficult or even impossible to distinguish the first from the second heart rate, even when using the technique of palpation of the apical impulse and the carotid artery.
Change in sonority (loudness) of heart sounds
A change in the sonority of tones can be in the form of an intensification or weakening (muffling) of both tones at all points of auscultation, either one of them, or at a separate point of auscultation (Fig. 337). All reasons that contribute to a change in the sonority of tones, both physiological and pathological, can be split into 2 groups

extracardiac;
cardiac.

Extracardiac reasons:

physical state of the body (long-term rest, physical, emotional stress);

-D-I

P
1x	T-
U and U p
	p G
0	and and
U

ECG
FCG, tones Normal tones
Strengthening I and II tones
Weakening of I and II tones
Weakening of the first tone
Weakening of the first tone in the aorta
Weakening of the first tone on the pulmonary artery
Sharp intensification of the first tone
Strengthening of the second tone on the aorta (emphasis)
Strengthening the second tone on the pulmonary artery (emphasis)

Rice. 337. Options for changing the sonority of heart sounds. Graphic image.

thickening or thinning of the chest wall;
condition of the lungs (bloating, thickening, cavity formation, wrinkling);
condition of the pleura (filling of the pleural cavity with liquid, air);
condition of the stomach (size of the gas bubble);
diaphragm level.

Cardiac reasons:

type of hemodynamics (hyperkinetic, hypokinetic, jy-kinetic);
acute and chronic cardiovascular failure;
condition of the pericardium (fusion of leaves, filling of the pericardium with air, liquid);
myocardial condition (hypertrophy, inflammation, dystrophy, cardiosclerosis);
condition of the valves (sealing, fusion of the valves, destruction of the valves);
condition of the main vessels (narrowing, dilation). Conventionally, the clinic distinguishes several gradations of sonority of tones:
loud tones;
the tones are very loud, amplified;
muffled tones - the sonority of the tones is reduced, weakened (the words “weakened tones” are not used in the presence of the patient);
dull tones - barely perceptible tones on auscultation;
no tones are heard.

The listed characteristics of tones can relate to both tones, one tone, or a tone at a separate listening point.
Variants of sonority of tones of a healthy person
The sonority of heart sounds in healthy people is extremely individual, which depends on a number of reasons.
Loud tones are heard in all healthy individuals under the age of 40-50 years.
Very loud (amplified) tones are heard in adolescents, asthenics with a thin chest wall, in emaciated individuals, during emotional and physical stress, which is associated with accelerated hemodynamics. The sonority of tones increases with deep exhalation and bending forward due to the approach of the heart to the chest wall. Very loud tones are possible in excitable individuals who have a hyperkinetic type of hemodynamics (increased frequency, strength and
rate of ventricular contraction), this is especially true for many young people.
Muted tones are heard in hypersthenics, in persons with highly developed muscles, an abundance of fat deposits, in women with significantly developed mammary glands. The reason for the muted tones is the thickening of the chest wall. Heart sounds become muffled in the horizontal position of the patient during prolonged rest, during sleep, or with deep inspiration, which is associated with the displacement of the heart back, moving away from the chest wall and greater coverage by the edges of the lungs.
The tones are very dull - they are not observed in healthy people.
A change in the sonority of one of the tones or at one of the listening points in a healthy person is observed relatively rarely. Strengthening the second tone on the aorta, that is, a louder sound on the aorta in comparison with the second sound on the pulmonary artery, is noted with a physiological, short-term increase in blood pressure, which happens with emotional and physical stress. A slight increase in the second rut on the aorta is observed in persons over 40 years old, especially in men. This is due to a slight increase in blood pressure at this age and hardening of the semilunar valves of the aorta. The predominance of the sound of the second tone on the aorta in comparison with the pulmonary artery, or vice versa, is called accent.
An increase in the second tone on the pulmonary artery in comparison with the second sound on the aorta is observed in adolescents (physiological emphasis). This is due to the fact that the pulmonary artery in children and adolescents lies closer to the chest wall than the aorta; in the pulmonary artery of adolescents, blood pressure is slightly higher than in adults. An increase in the second tone on the pulmonary artery appears during inspiration, especially in a horizontal position, which is associated with an increase in blood flow to the right side of the heart, an increase in blood ejection from the right ventricle, and, consequently, an increase in blood pressure in the pulmonary artery.
There is no weakening of individual tones in healthy people.
Changes in the sonority of both tones in pathology
Extracardiac causes Increased sounds with:

approach of the heart to the anterior chest wall (wrinkling of the edges of the lungs, swelling of the posterior mediastinum, high level of the diaphragm);
resonance of tones in large cavities of the lungs located adjacent to the heart, with left-sided pneumothorax, enlarged gas bubble of the stomach);
improving the conductivity of tones by the compacted edges of the lung next to the heart.

Weakening of tones with:

an increase in the thickness of the chest wall (obesity, swelling of the subcutaneous tissue in the heart area, subcutaneous emphysema, tumor of the chest wall);
covering the heart with emphysematous lungs;
distance of the apex of the heart from the chest wall by left-sided exudative pleurisy.

Cardiac causes Increased tones with:

hyperkinetic type of hemodynamics (neurocirculatory dystonia, hypertension);
tachycardia of any origin (fever, anemia, infectious diseases, pulmonary diseases, etc.),
I hyperthyroidism;
accumulation of gas in the pericardium (resonance).

Weakening of tones with:

acute cardiovascular failure;
myocardial damage (myocarditis, myocardiosclerosis, myocardial dystrophy);
damage to the pericardium (adhesive pericarditis, exudative pericarditis);
hypothyroidism.

Heart sounds are not heard in cases of pronounced pulmonary emphysema, severe myocarditis, exudative pericarditis, or in the agonal state of the patient.
Changing the sonority of the 1st or 2nd tone
A change in the sonority of one of the tones is mainly due to cardiac reasons.
Strengthening the 1st tone:

mitral stenosis (flapping 1st sound), which is caused by reduced blood filling of the left ventricle, high force and speed of contraction of the half-empty left ventricle, high speed of movement of the mitral valve leaflets;
strengthening of the first tone during extrasystolic contractions (contraction of a half-empty ventricle, a large degree of valve opening before systole);
“cannon tone” is a sharp, loud separate first sound that occurs with complete atrioventricular block and is caused by random simultaneous contraction of the atria and ventricles.

Weakening of the first tone (more common than intensification):

destruction of the mitral and tricuspid valves (incomplete closure of the valves during the isometric contraction phase);
relative mitral valve insufficiency;
aortic valve insufficiency (absence of a period of closed valves);
myocarditis, cardiosclerosis;
severe left ventricular hypertrophy;
decreased elasticity (fibrosis), calcification of the mitral valve leaflets;
atrioventricular block;
severe sinus bradycardia.

Change in sonority of tone II.
Strengthening of the second tone on the aorta:

hypertension of the systemic circulation of any origin;
sclerotic seal of the valve leaflets.

Weakening of the second tone on the aorta:

destruction of the aortic valves (defect - aortic insufficiency);
narrowing of the aortic mouth;
mitral stenosis;
left ventricular failure;
arterial hypotension.

Strengthening of the second tone on the pulmonary artery:

pulmonary hypertension of any origin: pulmonary diseases, impaired hemodynamics of the pulmonary circulation - narrowing, thrombosis of the branches of the pulmonary artery, mitral defects, congenital heart defects, myocarditis, acute myocardial infarction.

Weakening of the second tone on the pulmonary artery:

tricuspid stenosis or regurgitation;
pulmonary valve stenosis;
myocardial failure of the right ventricle.

Characteristics of heart sounds.

The opening of the valves is not accompanied by distinct vibrations, i.e. almost silently, and the closure is accompanied by a complex auscultation pattern, which is regarded as sounds I and II.

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

IItone 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 cusps of the mitral and tricuspid valves at the end of diastole and the beginning of systole, and the initial oscillation is observed when the cusps of the mitral valve are closed, and the final oscillation is observed when the cusps of the tricuspid valve are closed, therefore the mitral and tricuspid components are distinguished;

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

vascular component– low-amplitude oscillations that occur at the moment 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 the blood flow moving from the ventricles to the great vessels at the beginning of ventricular systole (the ejection period). These oscillations occur after the valve component at approximately 0.02 seconds;

atrial component– low-amplitude oscillations resulting from atrial systole. This component precedes the valve component of the first tone. It is detected only in the presence of mechanical atrial systole, disappears with atrial fibrillation, nodal and idioventricular rhythm, AV block (absence 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. It begins diastole and ends systole. Comprises 2 components:

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

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

When analyzing heart sounds, it is necessary to determine them quantity, find out what tone is first. At a normal heart rate, the solution to this problem is clear: the first sound occurs after a longer pause, i.e. diastole, II tone – after after a short pause, i.e. systole. For 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 in 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 increased strength, during physical and mental stress), additional III and IV tones (physiological) appear. Their appearance is associated with vibrations 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 second sound. It is better heard by direct auscultation at the apex of the heart. It is a weak, low, short sound. It is a sign of good development of the ventricular myocardium. With an increase in the tone of the ventricular myocardium in the phase of rapid filling in ventricular diastole, the myocardium begins to oscillate and vibrate. It is heard 0.14 -0.20 after the second tone.

IV tone is presystolic, because appears at the end of diastole, precedes the first sound. Very quiet, short sound. It is heard in individuals with increased ventricular myocardial tone and is caused by fluctuations in the ventricular myocardium when blood enters them during atrial systole. Most often heard in an upright 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 nervous system, there is some advance of contractions of the atria from the ventricles and therefore the fourth component of the 1st sound begins to be heard separately from the 1st tone and is called the 4th tone.

FeaturesIAndIItones.

The first sound is heard louder at the apex and at the tricuspid valve at the base of the xiphoid process at the beginning of systole, that is, after a long pause.

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

The first tone is longer, but lower, duration is 0.09-0.12 seconds.

II tone is higher, short, duration 0.05-0.07 seconds.

The tone that coincides with the apex beat and the pulsation of the carotid artery is the 1st tone, the 2nd tone does not coincide.

The first tone does not coincide with the pulse in 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 location of the apex beat. At this point, a sound vibration is heard that occurs when the mitral valve operates;

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

II intercostal space, to the left of the sternum. The pulmonary valve is heard here;

area 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. Sound vibrations that occur during the operation of the aortic valve, less often the mitral and tricuspid valves, are heard here.

During auscultation, the points of maximum sound of heart sounds are determined:

I tone – area of the apex of the heart (I tone is louder than II)

II tone – area of the base of the heart.

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

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

During auscultation they analyze sonority heart sounds, which depends on the summative effect of extra- and intracardial factors.

TO extracardiac factors include the thickness and elasticity of the chest wall, age, body position, and intensity of pulmonary ventilation. Sound vibrations are better transmitted through the thin elastic chest wall. Elasticity is determined by age. In a vertical position, the sonority of heart tones is greater than in a horizontal position. At the height of inhalation, sonority decreases, while exhaling (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 position of the diaphragm (with ascites, in pregnant women, with moderate obesity), the heart “presses” more against the anterior chest wall, and the sonority of heart sounds increases.

The sonority of heart sounds 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 sounds decreases (with emphysema), with a decrease in the airiness of the lung tissue, the sonority of the heart sounds increases (with wrinkling of the lung tissue, surrounding the heart).

With cavity syndrome, heart sounds may acquire metallic shades (sonority increases) if the cavity is large and has tense walls.

The accumulation of fluid in the pleural strip and in the pericardial cavity is accompanied by a decrease in the sonority of heart sounds. 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 sounds increases (due to the resonance of sound vibrations in the air cavity).

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

the nature of the neurovegetative regulation of the cardiovascular system as a whole (the ratio of the tone of the sympathetic and parasympathetic sections of the ANS);

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

Highlight 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 ventricular contraction, an increase in the speed of blood flow, which is accompanied by an increase in the sonority of heart sounds;

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

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

For heart pathology intracardial factors include:

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

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;

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

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

A change in the first and second sounds is observed with aortic defects, arrhythmias, and AV conduction disorders.

For aortic insufficiency The sonority of the second tone at the base of the heart and the first tone at the apex of the heart decreases. The decrease in the sonority of the second tone is associated with a decrease in the amplitude of the valve 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 moment of their slamming. Reducing sonorityItones is associated with a decrease in valve oscillations (oscillation - amplitude) of the first tone, which is observed with pronounced dilatation of the left ventricle in aortic insufficiency (the aortic opening expands, relative mitral insufficiency develops). The muscle component of the first tone also decreases, which is due to the absence of a period of isometric tension, because there is no period of complete valve closure.

For aortic stenosis a decrease in the sonority of the first and second sounds at 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 a change in the diastolic volume of the ventricle. As the duration of diastole increases, blood volume increases, which is accompanied by decreased sonority of heart sounds at all auscultatory points.

For bradycardia diastolic overload is observed, therefore a decrease in the sonority of heart sounds at all auscultatory points is characteristic; with tachycardia diastolic volume decreases and sonority increases.

In case of pathology of the valve apparatus an isolated change in the sonority of the first or second tone is possible.

With stenosis,AVblockadeAVarrhythmias The sonority of the first tone increases.

For mitral stenosis I tone clapping. This is due to an increase in the diastolic volume of the left ventricle, and since the load falls on the left ventricle, and there is a discrepancy between the strength of contractions of the left ventricle and the volume of blood. There is an increase in distance mileage, because BCC decreases.

With a decrease in elasticity (fibrosis, Sanosis), the mobility of the valves decreases, which leads to reduction of sonorityItones.

With complete AV block, which is characterized by different rhythms of contraction of the atria and ventricles, a situation may arise when the atria and ventricles contract simultaneously - in this case, increase in sonorityItones at the apex of the heart - "cannon" tone Strazhesko.

Isolated attenuationItones observed in organic and relative mitral and tricuspid insufficiency, which is characterized by changes in the leaflets of these valves (previous rheumatism, endocarditis) - deformation of the leaflets, which causes incomplete closure of the mitral and tricuspid valves. As a result, a decrease in the amplitude of oscillation of the valve component of the first tone is observed.

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

Complete destruction of the mitral or tricuspid valve leads to disappearanceItones - at the apex of the heart,IItones - in the area of the base of the xiphoid process.

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

Physiological change in tone II ( sonority enhancement) above the pulmonary artery is observed in children, adolescents, and young people, especially during physical activity (physiological increase in pressure in the ICC).

In older people sonority enhancementIItones above the aorta associated with an increase in pressure in the BCC with pronounced thickening of the vessel walls (atherosclerosis).

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

Reducing sonorityIItones above the pulmonary artery is determined with tricuspid insufficiency.

Changing the volume of heart sounds. They can occur in strengthening or weakening, can be simultaneously for both tones or isolated.

Simultaneous weakening of both tones. Causes:

1. extracardiac:

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

Left-sided effusion pericarditis

Emphysema

2. intracardial - decreased 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 sound, in the aorta and pulmonary artery the volume of incoming blood decreases, which means the second sound weakens.

Simultaneous volume boost:

Thin chest wall

Wrinkling of the pulmonary edges

Increasing the diaphragm position

Space-occupying formations in the mediastinum

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

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

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

GainItones.

Mitral stenosis – flapping sound. The blood volume at the end of diastole in the LV decreases, which leads to an increase in the rate of myocardial contraction, and the mitral valve leaflets thicken.

Tachycardia

Extrasystole

Atrial fibrillation, tachyform

Incomplete AV block, when the contraction of the P-th coincides with the contraction of the Zh-ov - Strazhesko’s cannon tone.

WeakeningItones:

Mitral or tricuspid valve insufficiency. The absence of closed valves leads to a sharp weakening of the valve and muscle components

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

Stenosis of the aortic mouth - the first sound weakens due to pronounced 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 the second tone also decreases.

If at the top the I tone is equal in volume to the II or louder than the II tone, the I tone is weakened. The first tone is never analyzed based on the heart.

Changing the volumeIItones. The pressure in the PA 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 people under 25 years of age, there is a functional strengthening (emphasis) of the second tone over the LA. The reason is the more superficial location of the pulmonary valve and the higher elasticity of the aorta, lower pressure in it. With age, blood pressure in the BCC increases; The PA moves posteriorly, the accent of the 2nd tone above the LA disappears.

Reasons for strengtheningIItones above the aorta:

Increased blood pressure

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

Reasons for strengtheningIItones over LA– increased pressure in the BCC with mitral heart defects, chronic respiratory diseases, primary pulmonary hypertension.

WeakeningIItones.

Above the aorta: - aortic valve insufficiency - absence of a period of closure (?) 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 shortening of diastole and small cardiac ejection of blood into the aorta

Severe arterial hypertension

Reasons for weakeningIItones on LA– insufficiency of the pulmonary valves, stenosis of the orifice of the pulmonary artery.

Splitting and splitting 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 detect this time difference; we hear the work of the right and left ventricles as single tones.

If the asynchrony time increases, then each tone is not perceived as a single sound. On the FCG it is recorded within 0.02-0.04 seconds. Splitting is a more noticeable doubling of tone, asynchrony time is 0.05 sec. and more.

The reasons for splitting tones and splitting are the same, the difference is in time. Functional split tone can be heard at the end of expiration, when intrathoracic pressure increases 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 auscultation of the cleft.

Pathological bifurcation of the first tone occurs as a result of delayed excitation of one of the ventricles during blockade of one of the branches of the His bundle, this leads to delayed contraction of one of the ventricles or with ventricular extrasystole. Severe myocardial hypertrophy. One of the ventricles (usually the left one - with aortic hypertension, aortic stenosis) the myocardium is excited later and contracts more slowly.

BifurcationIItones.

Functional bifurcation is more common than the first, occurring in young people at the end of inhalation or the beginning of exhalation, during physical activity. The reason is the non-simultaneous end of systole of the left and right ventricles. Pathological bifurcation of the second tone is more often observed in the pulmonary artery. The reason is an increase in pressure in the ICC. As a rule, an increase in the second tone in the pulmonary artery is accompanied by a bifurcation of the second tone in the pulmonary artery.

Additional tones.

In systole, additional tones appear between the I and II sounds; this, as a rule, is a tone called a systolic click, which appears when the mitral valve prolapses (sagging), caused by prolapse of the mitral valve leaflet during systole into the left atrium cavity - a sign of connective tissue dysplasia. It is often heard in children. The systolic click can be early or late systolic.

In diastole during systole, the third pathological sound, the fourth pathological tone and the sound of the opening of the mitral valve appear. IIIpathological tone occurs after 0.12-0.2 seconds. from the beginning of the second 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 if the ventricular myocardium has lost its tone, therefore, when the ventricular cavity is filled with blood, the muscle easily and quickly stretches, the ventricular wall vibrates, and a sound is produced. It is heard in case of severe myocardial damage (acute myocardial infections, severe myocarditis, myocardial dystrophy).

PathologicalIVtone occurs before the first sound at the end of diastole in the presence of overcrowded atria and a sharp decrease in ventricular myocardial tone. Rapid stretching of the wall of the ventricles, which have lost their tone, when a large volume of blood enters them in the atrial systole phase causes myocardial vibrations and a fourth pathological tone appears. III and IV sounds are better heard at the apex of the heart, on the left side.

Gallop rhythm first described by Obraztsov in 1912 – "cry of the heart for help". It is a sign of a sharp decrease in myocardial tone and a sharp decrease in the contractility of the ventricular myocardium. So named because it resembles the rhythm of a galloping horse. Signs: tachycardia, weakening of the 1st and 2nd sounds, the appearance of pathological 3rd or 4th sounds. Therefore, protodiastolic (three-part rhythm due to the appearance of the third tone), presystolic (third tone at the end of diastole due to the fourth pathological tone), mesodiastolic, summation (with severe tachycardia, the third and fourth sounds merge, a summation third tone is heard in the middle of diastole) are distinguished.

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

Pendulum-shapedrhythm– the melody of the heart is relatively rare, when due to diastole both phases are balanced 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 pendular rhythm is accompanied by tachycardia, this indicates embryocardia, that is, the melody resembles the heartbeat of a fetus.

Heart sounds are the sum of various sound phenomena that occur during the cardiac cycle. Usually two tones are heard, but in 20% of healthy individuals the 3rd and 4th tones are heard. With pathology, the characteristics of tones change.

The 1st sound (systolic) is heard at the beginning of systole.

There are 5 mechanisms for the appearance of the 1st tone:

The valvular component arises from the sound phenomenon that occurs when the mitral valve closes at the beginning of systole.
Oscillations and closure of the tricuspid valve leaflets.
Oscillations of the walls of the ventricles during the phase of isometric contraction at the beginning of systole, when the heart pushes blood into the vessels. This is the muscle component of the 1st tone.
Fluctuations in the walls of the aorta and pulmonary artery at the beginning of the expulsion period (vascular component).
Fluctuations of the atrial walls at the end of atrial systole (atrial component).

The first tone is normally heard at all auscultation points. The place of his assessment is the apex and Botkin's point. The assessment method is comparison with the 2nd tone.

The 1st tone is characterized by the fact that

a) occurs after a long pause, before a short one;

b) at the apex of the heart it is greater than the 2nd tone, longer and lower than the 2nd tone;

c) coincides with the apex beat.

After a short pause, a less sonorous 2nd tone begins to be heard. The 2nd sound is formed as a result of the closure of two valves (aorta and pulmonary artery) at the end of systole.

There are mechanical systole and electrical systole, which does not coincide with the mechanical one. The 3rd tone can be present in 20% of healthy people, but more often in sick individuals.

The physiological 3rd sound is formed as a result of vibrations of the walls of the ventricles during their rapid filling with blood at the beginning of diastole. Usually observed in children and adolescents due to the hyperkinetic type of blood flow. The 3rd sound is recorded at the beginning of diastole, no earlier than 0.12 seconds after the 2nd sound.

The pathological 3rd tone forms a three-part rhythm. It occurs as a result of rapid relaxation of the muscles of the ventricles that have lost their tone with the rapid flow of blood into them. This is the “cry of the heart for help” or the rhythm of a gallop.

The 4th tone can be physiological, occurring before the 1st tone in the diastole phase (presystolic tone). These are vibrations of the walls of the atria at the end of diastole.

Normally it occurs only in children. In adults, it is always pathological, caused by contraction of the hypertrophied left atrium with loss of ventricular muscle tone. This is the presystolic gallop rhythm.

During auscultation, clicks can also be heard. A click is a high-pitched sound of low intensity heard during systole. Clicks are characterized by high pitch, shorter duration and mobility (inconstancy). It is better to listen to them with a phonendoscope with a membrane.