Thromboembolism of the systemic and pulmonary circulation. Pulmonary embolism: diagnosis, treatment and prevention

Date: 03.03.2020

Heart valve	Topographic projection	Listening points
Mitral (bivalve)	to the left of the sternum, the area of attachment of the cartilage of the III rib	apex of the heart
Tricuspid	on the sternum, the middle of the distance between the place of attachment of the cartilage of the III rib on the left and the cartilage of the V rib on the right	the lower end of the sternum, at the base of the xiphoid process of the sternum
Aortic	in the middle of the sternum, at the level of 3 costal cartilages	II intercostal space, to the right of the sternum
on the left at the sternum, the place of attachment of the cartilage of 3-4 ribs (V so - additional listening point of the aortic valve - Botkin-Erb point)
Pulmonary		II intercostal space, to the left of the sternum

Rules for auscultation of the heart:

1. The room in which the auscultation is performed should be quiet and warm.

2. The position of the patient is horizontal and vertical, if necessary, auscultation is performed after physical exertion.

NB! It is better to listen to the sound phenomena associated with the pathology of the mitral valve in the position on the left side, and the aortic one - in the vertical and slightly tilted forward position with arms raised upward or in the supine position on the right side.

3. Auscultation of the heart is performed both with calm shallow breathing of the patient, and with holding the breath after maximum exhalation.

4. To synchronize sound phenomena with the phases of systole and diastole, it is necessary to simultaneously palpate the patient's right carotid artery with the left hand, the pulsation of which practically coincides with the ventricular systole.

5. The order of auscultation of the heart is as follows:

1) at the apex of the heart - the point of auscultation of the mitral valve

2) in the II intercostal space to the right of the sternum - i.e. aortic valve

3) in the II intercostal space to the left of the sternum - i.e. pulmonary valve

4) at the base of the xiphoid process, also to the left and right of it - i.e. tricuspid valve

5) IV intercostal space - Botkin-Erb point - additional t.a. aortic valve.

Changes in heart sounds are manifested in:

1) weakening or increasing the sonority of one or both tones

2) changing the duration of tones

3) the appearance of bifurcation or splitting of tones

4) the appearance of additional tones

Changing tones, listening places	Mechanism	Diseases in which this phenomenon manifests itself
Weakening the sonority of both tones	Extra-heart reasons	Distance of the heart from the anterior chest wall	1) strong development of subcutaneous fatty tissue or pectoral muscles 2) emphysema of the lungs 3) hydrothorax
Cardiac causes	Decreased contractility of the myocardium	1) myocarditis 2) myocardial dystrophy 3) acute myocardial infarction 4) cardiosclerosis 5) hydropericardium
Enhancing the sonority of both tones	Extra-heart reasons	Approaching the heart to the anterior chest wall	1) thin chest wall 2) wrinkling of the edges of the lungs 3) tumor in the posterior mediastinum
Resonance of tones due to adjacent cavities	1) large pulmonary cavity 2) large gas bubble of the stomach
Change in blood viscosity	1) anemia
Cardiac causes	Strengthening the contractile function due to the increased influence of the sympathetic NA	1) hard physical work 2) emotional stress 3) Graves' disease
Weakening of the I tone	At the top of the heart	1. Prolongation of the PR interval (first degree AV block) 2. Mitral insufficiency 3. Severe mitral stenosis 4. "Rigid" left ventricle (with arterial hypertension)	1) mitral valve insufficiency 2) aortic valve insufficiency 3) narrowing of the aortic orifice 4) diffuse myocardial damage: myocarditis, cardiosclerosis, dystrophy
	1) failure of the 3-leaf valve 2) failure of the pulmonary valve
Amplification of I tone	At the top of the heart	1. Shortened PR interval 2. Moderate mitral stenosis 3. Increased CO or tachycardia (exercise, anemia)	1) stenosis of the left AV hole (loud flapping I tone)
At the base of the xiphoid process	1) stenosis of the right AV opening 2) tachycardia 3) extrasystole 4) thyrotoxicosis
Attenuation of II tone	Above the aorta	1. Violation of the tightness of the closure of the semilunar valves. 2. Decrease in the rate of closure of the semilunar valves in heart failure and decrease in blood pressure 3. Fusion and decrease in the mobility of the semilunar valves in valve stenosis of the aortic orifice	1) insufficiency of the aortic valve (destruction of the valve leaflets, scar) 2) significant decrease in blood pressure
Above the pulmonary trunk	1) insufficiency of the pulmonary valve 2) decrease in pressure in the ICC
Gain II tone	Above the aorta (emphasis on the aorta)	1. Increase in blood pressure of various genesis 2. Compaction of the aortic valve cusps and aortic walls 3. Overflow of blood vessels of the ICC in mitral heart diseases 4. Obstruction of blood circulation in the lungs and narrowing of the pulmonary artery bed	1) hypertension 2) hard physical work 3) psychoemotional arousal 4) aortic valve sclerosis (metallic shade)
Above the pulmonary artery (focus on the pulmonary artery)	1) mitral stenosis 2) cor pulmonale 3) left ventricular heart failure 4) pulmonary emphysema 5) pneumosclerosis
Bifurcation of the second tone - an increase in the time interval between A2 and P2 (aortic and pulmonary) components, while the components clearly differ even on inhalation, on exhalation the interval between them increases a) blockade of PNPH b) pulmonary artery stenosis Fixed splitting of the second tone - increased interval between A 2 and P 2, which remains unchanged during the respiratory cycle: atrial septal defect. Paradoxical (reverse) splitting of the second tone - clearly audible splitting of A2 and P2 on inspiration, disappearing on expiration: a) blockade of LPH b) severe aortic stenosis
Bifurcation of I tone	Physiological	Non-simultaneous closing of AV valves	During a very deep breath
Pathological	Delay of systole of one of the ventricles	Violation of intraventricular conduction (along the legs of the bundle of His)
Bifurcation of II tone	Physiological	Change in ventricular blood flow during inspiration and expiration	Inhalation → decrease in the amount of blood flowing to the LV (due to blood retention in the dilated vessels of the lungs) → LV systolic volume decreases → the aortic valve closes earlier
Pathological	1) Decrease or increase in blood filling of one of the ventricles 2) Change in pressure in the pulmonary artery or aorta	1) stenosis of the orifice of the aorta (lagging behind the collapse of the aortic valve) 2) hypertension 3) mitral stenosis (lagging behind the collapse of the pulmonary valve with increased pressure in the ICC) 4) blockade of the bundle branch (lagging behind the contraction of one of the ventricles)
NB! Pathological splitting of I and II tones is more pronounced and is heard during inhalation and exhalation, physiological - during a deep inhalation.
Additional tones and rhythms.
III tone	A significant drop in the contractility (and diastolic tone) of the ventricular myocardium	1) heart failure 2) acute myocardial infarction 3) myocarditis
Significant increase in atrial volume	1) mitral valve insufficiency 2) tricuspid valve insufficiency
Increased diastolic tone with severe vagotonia	1) neurosis of the heart 2) peptic ulcer and 12 duodenal ulcer
Increased diastolic rigidity of the ventricular myocardium	1) severe myocardial hypertrophy 2) cicatricial changes
IV tone	Significant decrease in myocardial contractility	1) acute heart failure 2) acute myocardial infarction 3) myocarditis
Severe ventricular myocardial hypertrophy	1) stenosis of the aortic orifice 2) hypertension
mitral valve opening tone	Blow of blood from the atrium against the sclerosed mitral valve	mitral stenosis (detected during diastole 0.07-0.13 after tone II)
quail rhythm ("sleep-by-ra")	I (loud clapping) tone with mitral stenosis + II tone + tone of opening of the mitral valve	sign of mitral stenosis
pericardial tone	Pericardial oscillations with rapid expansion of the ventricles during systole	fusion of the pericardium (detected during diastole 0.08-0.14 s after tone II)
systolic click: a loud short tone between I and II during systole	The impact of a portion of blood on the sealed wall of the ascending aorta at the very beginning of the period of expulsion of blood from the LV	1) atherosclerosis of the aorta 2) hypertension EARLY SYSTOLIC CLICK
Mitral leaflet prolapse into the LA cavity in the middle or at the end of the expulsion phase	1) mitral valve prolapse MESOSYSTOLIC OR LATE SYSTOLIC CLICK
three-membered gallop rhythm a) protodiastolic b) presystolic c) mesodiastolic (summarized)	It is heard better a) directly by the ear b) after moderate physical. load c) in the position of the patient on the left side	Strengthening the physiological III or IV tone.
Significant decrease in the tone of the ventricular myocardium → filling the ventricles with blood during diastole → faster stretching of the walls and the appearance of sound vibrations	It occurs 0.12-0.2 s after the II tone (physiologically enhanced tone III) at the beginning of diastole.
Decreased ventricular myocardial tone and stronger atrial contraction	In the middle of diastole, physiologically enhanced IV tone
Severe myocardial damage.	A single gallop rhythm in the middle of diastole, intensified III and IV tones, merging together with tachycardia 1) myocardial infarction 2) hypertension 3) myocarditis, cardiomyopathy 4) chronic nephritis 5) decompensated heart defects
Embryocardia (pendulum rhythm)	A sharp increase in heart rate → shortening the diastolic pause to the duration of the systolic → fetal heart sounds or the clock	1) acute heart failure 2) an attack of paroxysmal tachycardia 3) high fever

abstract

On the topic: "Borders of the heart and the projection of the heart valves"

Content

The structure and location of the heart, its relation to the walls of the chest

Blood supply, innervation and lymph drainage of the heart
Heart valve projections
Physical methods of research of the heart
List of used literature

The structure and location of the heart its relation to the walls of the chest

heart blood supply innervation lymph drainage

The heart (Latin cor, Greek cardia) is a hollow fibromuscular organ that, functioning as a pump, ensures the movement of blood in the circulatory system.

The heart is located in the anterior mediastinum in the pericardium between the leaves of the mediastinal pleura. It has the shape of an irregular cone with a base at the top and a top facing downward, to the left and anteriorly. The size of the heart is individually different. The length of the heart of an adult varies from 10 to 15 cm (usually 12-13 cm), the width at the base is 8-11 cm (usually 9-10 cm) and the anteroposterior size is 6-8.5 cm (usually 6, 5 --7 cm). The average heart weight in men is 332 g (from 274 to 385 g), in women - 253 g (from 203 to 302 g).

In relation to the midline of the body, the heart is located asymmetrically - about 2/3 to the left of it and about 1/3 to the right. Depending on the direction of the projection of the longitudinal axis (from the middle of its base to the apex) on the anterior chest wall, a transverse, oblique and vertical position of the heart is distinguished. The upright position is more common in people with a narrow and long chest, transverse - in people with a wide and short chest.

The heart consists of four chambers: two (right and left) atria and two (right and left) ventricles. The atria are located at the base of the heart. The aorta and the pulmonary trunk emerge from the heart in front, the superior vena cava flows into it in the right part, the inferior vena cava flows into the posterior inferior, the left pulmonary veins are in the back and left, and the right pulmonary veins are somewhat to the right. Distinguish between the anterior (sternocostal), lower (diaphragmatic), which in the clinic is sometimes called the posterior, and the left lateral (pulmonary) surface of the heart. The right edge of the heart is also distinguished, formed mainly by the right atrium and adjacent to the right lung. The anterior surface, adjacent to the sternum and cartilage of the left III-V ribs, is represented over a greater extent by the right ventricle, on a smaller one - by the left ventricle and atria. The border between the ventricles corresponds to the anterior interventricular groove, and between the ventricles and the atria - the coronary groove. In the anterior interventricular sulcus, the anterior interventricular branch of the left coronary artery, the great vein of the heart, the nerve plexus and the diverting lymphatic vessels are located; in the coronary sulcus, the right coronary artery, nerve plexus and lymphatic vessels. The diaphragmatic surface of the heart faces downward and is adjacent to the diaphragm. It is composed of the left ventricle, partly the right ventricle, and sections of the right and left atria. On the diaphragmatic surface, both ventricles border each other along the posterior interventricular groove, in which the posterior interventricular branch of the right coronary artery, the middle vein of the heart, nerves and lymphatic vessels pass. The posterior interventricular groove near the apex of the heart connects with the anterior one, forming a notch of the apex of the heart. The silhouette of the frontal projection of the heart onto the anterior chest wall has right, lower and left borders. The right border is formed at the top (II - III rib) by the edge of the superior vena cava, below (III - V rib) - by the edge of the right atrium. At the level of the V rib, the right border passes into the lower one, which is formed by the edge of the right and partially left ventricles and goes obliquely down and to the left, crossing the sternum above the base of the xiphoid process, to the intercostal space on the left and further, crossing the cartilage of the VI rib, reaches the V intercostal space by 1 , 5 cm medially from the midclavicular line. The left border is formed by the aortic arch, the pulmonary trunk, the left ear of the heart and the left ventricle. The exit sites of the aorta and the pulmonary trunk are projected at the level of the III intercostal space: the aortic mouth is behind the left half of the sternum, and the pulmonary trunk mouth is at its left edge.

The structure of the chambers of the heart is consistent with its function as a pump. The right atrium with the right ventricle, the left one with the left, communicates, respectively, through the right and left atrioventricular openings, equipped with valves that ensure the direction of blood flow from the atria to the ventricles during their diastole and prevent backflow during ventricular systole. The communication of the cavities of the ventricles with the arteries is regulated by valves located in the orifices of the aorta and the pulmonary trunk. The right atrio-gastric valve is called tricuspid (tricuspid), the left - bicuspid, or mitral.

The right atrium has an irregular cubic shape; its capacity in an adult ranges from 100-140 ml, the wall thickness is 2-3 mm. On the right, the atrium forms a hollow process - the right ear. Its inner surface has a number of ridges formed by bundles of comb muscles. On the lateral wall of the atrium, the comb muscles end, forming an elevation - the border ridge (crista terminalis), which on the outer surface corresponds to the border groove (sulcus terminalis). The medial wall of the atrium - the interatrial septum - has an oval fossa in the center, the bottom of which is formed, as a rule, by two sheets of the endocardium. The height of the fossa is 18-22 mm, the width is 17-21 mm.

The shape of the right ventricle approaches a trihedral pyramid (base facing upwards), the medial wall of which belongs to the interventricular septum. The capacity of the right ventricle in adults is 150-240 ml, the wall thickness is 5-7 mm. The weight of the right ventricle is 64-74 g. In the right ventricle, two parts are distinguished: the ventricle itself and the arterial cone, located in the upper left part of the ventricle and continuing into the pulmonary trunk. The diameter of the opening of the pulmonary trunk is 17-21 mm. Its valve consists of 3 semi-moon flaps: front, right and left. In the middle of each semilunar flap, there are nodules (nodules) that contribute to a more hermetic closing of the flaps. The inner surface of the ventricle is uneven due to fleshy trabeculae extending in different directions, which are poorly expressed on the interventricular septum. The right atrioventricular (atrioventricular) opening, located at the top of the ventricle (to the right and behind the opening of the pulmonary trunk), has an oval shape; its longitudinal size is 29-48 mm, transverse - 21-46 mm. The valve of this opening, like the mitral valve, consists of an annulus fibrosus; the valves, which attach their base to the annulus fibrosus (the free edges of the valves face the cavity of the ventricle); tendinous chords extending from the free edges of the valves to the wall of the ventricle, to the papillary muscles or fleshy trabeculae; papillary muscles formed by the inner layer of the ventricular myocardium. The number of valve cusps only slightly more often than in half of the cases corresponds to its designation "tricuspid"; it ranges from 2 to 6, with a greater number of valves found with large sizes of the atrioventricular opening. At the point of attachment, the anterior, posterior and septal valves and the corresponding papillary muscles are distinguished, with the tops of which the valves are connected by tendon chords. A large number of papillary muscles occurs with an increased number of valves.

The left atrium, which is close to a cylindrical shape, forms an outgrowth on the left - the left ear. The capacity of the left atrium is 90-135 ml, wall thickness is 2-3 mm. The inner surface of the atrial walls is smooth, except for the walls of the ear, where there are ridges of the comb muscles. On the back wall there are the mouths of the pulmonary veins (two to the right and two to the left). On the interatrial septum from the left atrium, the valve of the oval opening (valvula foraminis ovalis) fused with the septum is noticeable. The left ear is narrower and longer than the right one; it is delimited from the atrium by a well-defined intercept.

The left ventricle is tapered. Its capacity is from 130 to 220 ml, wall thickness is 11-14 mm. The mass of the left ventricle is 130-150 g. Because of the roundness of the left edge of S., the anterior and posterior walls of the left ventricle are not sharply demarcated, the medial wall corresponds to the interventricular septum. The area of the left ventricle closest to the opening of the aorta is called the arterial cone. The inner surface of the ventricle, with the exception of the septum, has numerous fleshy trabeculae. At the top there are two openings: on the left and in front - the oval left atrioventricular (its longitudinal size is 23-37 mm, transverse - 17-33 mm), on the right and back - the opening of the aorta. The valve of the left atrioventricular opening (mitral) most often has two cusps and, accordingly, two papillary muscles - anterior and posterior. The aortic valve is formed by three semilunar valves - posterior, right and left. The initial part of the aorta at the location of the valve is expanded (its diameter reaches 22-30 mm) and has three depressions - the sinuses of the aorta.

The walls of the heart are formed by three membranes: the outer one is the epicardium, the inner one is the endocardium and the muscular membrane located between them is the myocardium. The epicardium - the visceral plate of the pericardium - is the serous membrane. It consists of a thin plate of connective tissue with a different arrangement of elastic and collagen fibers, covered from the surface with mesothelium. The myocardium (Fig. 5) makes up the bulk of the heart wall. The ventricular myocardium is separated from the atrial myocardium by fibrous rings, from which the bundles of myocardial fibers begin. In the myocardium of the ventricles, it is conditionally possible to distinguish the outer, middle and inner (deep) layers. The outer layers of the ventricular myocardium are common. The course of the fibers of the outer and inner layers has the form of a rare spiral; the middle layer of the bundles of the myocardium is circular. Histologically, myocardial tissue differs from striated skeletal muscle tissue in a number of features, incl. smaller sizes of myocardial cells (cardiomyocytes) and sarcomeres, the presence of one nucleus in the cell, connecting cardiomyocytes in series with each other in an end-to-end manner by means of insertion disks, etc. About 30-40% of the volume of cardiomyocytes is occupied by mitochondria. The particular saturation of cardiomyocytes with mitochondria reflects the high metabolic rate of tissue with continuous activity. In the myocardium there is a special system of fibers that have the ability to conduct impulses to all muscle layers of C. and coordinate the sequence of contraction of the wall of the chambers C. These specialized muscle fibers make up the conducting system of the heart. It consists of sinus-atrial and atrioventricular nodes and bundles (atrial, internodal connective, atrioventricular and its branches, etc.). In the tissue of the S.'s conducting system, which is more adapted to anaerobic metabolism than the contractile myocardium, mitochondria occupy about 10% of the cell volume, and myofibrils - about 20%. The endocardium lines the S. cavity, including the papillary muscles, tendon chords, trabeculae and valves. In the ventricles, the endocardium is thinner than in the atria. It, like the epicardium, consists of two layers: subendothelial and collagen-elastic, covered with endothelium. The leaflet of the heart valve is a fold of the endocardium, in which there is a connective tissue layer.

The ratio of the heart and its parts to the anterior chest wall changes depending on the position of the body and breathing movements. So, when the body is on the left side or in an anteriorly inclined state, the heart is closer to the chest wall than in opposite body positions; when inhaling, it is farther from the chest wall than when exhaling. In addition, the position of the heart changes depending on the phases of cardiac activity, on age, gender and individual characteristics. The heart lies behind the lower half of the sternum, and the large vessels lie behind the upper half. The left venous opening (bicuspid valve) lies to the left of the sternum in the third intercostal space; the work of the valve is heard at the apex of the heart. The right venous opening (tricuspid valve) is projected behind the sternum on a line drawn from the cartilage of the III rib on the left to the cartilage of the V rib on the right; the work of the valve is heard at the edge of the sternum in the fourth intercostal space on the right.

Blood supply, innervation and lymph drainage of the heart

The innervation of the heart comes from the cardiac plexus, located under the epicardium, mostly in the walls of the atria, less in the walls of the ventricles. It is formed by the branches of the thoracic aortic plexus, and also has cardiac ganglia containing synapses of pre- and postganglionic parasympathetic nerve fibers. As part of the branches of the thoracic aortic plexus, postganglionic sympathetic, preganglionic parasympathetic and sensory nerve fibers are suitable for S. Fibers of the cardiac plexus form secondary intramural plexuses with sensory and nictitating fibers.

The blood supply to the heart is usually carried out by the right and left coronary arteries extending from the aortic bulb. Depending on the predominant value of any of them in supplying the heart with blood, right-coronary and left-coronary arteries are distinguished, as well as uniform types of blood supply. The left coronary artery is divided into the enveloping and anterior interventricular branches. Several branches depart from the circumflex artery, incl. anastomotic anterior, atrioventricular, left marginal, intermediate atrial, posterior left ventricle, as well as branches of the sinus-atrial and atrioventricular nodes and atrial branches. The branches of the arterial cone, lateral and septal interventricular branches are separated from the anterior interventricular artery. The right coronary artery gives off a branch of the arterial cone, branches of the sinus-atrial and atrioventricular nodes, atrial and intermediate atrial branches, the right marginal, posterior interventricular (septal interventricular branches depart from it) and the right posterolateral branch. S.'s arteries branch in all its membranes. Thanks to anastomoses in S. there can be collateral circulation. The outflow of blood from the veins of the wall S. occurs mainly in the coronary sinus, which flows into the right atrium. In addition, blood flows directly into the right atrium through the anterior veins of the heart.

Lymphatic drainage is carried out from the endocardial lymphocapillary network to the myocardial vessels, and from the myocardial and epicardial networks to the subepicardial lymphatic vessels. From them, the right and left main lymphatic vessels are formed, which flow into the lymph nodes of the mediastinum.

Heart valve projections

Right border of the heart formed by the right surface of the superior vena cava and the edge of the right atrium. It runs from the upper edge of the cartilage of the right II rib at the place of its attachment to the sternum to the upper edge of the cartilage of the III rib 1.0-1.5 cm outward from the right edge of the sternum. Then the right border of the heart, corresponding to the edge of the right atrium, runs arcuate from ribs III to V at a distance of 1-2 cm from the right edge of the sternum.

V ribs right border of the heart passes into the lower border of the heart, which is formed by the edges of the right and partially left ventricles. The lower border runs along an oblique line down and to the left, crosses the sternum above the base of the xiphoid process, then goes to the sixth intercostal space on the left and through the cartilage of the VI rib into the fifth intercostal space, not reaching the mid-clavicular line by 1--2 cm.The apex is projected here hearts.

The left border of the heart is made up of the aortic arch, pulmonary trunk, left ear and left ventricle. From the apex of the heart, it runs in a convex outward arc to the lower edge of the III rib 2-2.5 cm to the left of the edge of the sternum. At the level of the third rib, it corresponds to the left ear. Rising upward, at the level of the second intercostal space, it corresponds to the projection of the pulmonary trunk. At the level of the upper edge of the II rib, 2 cm to the left of the edge of the sternum, it corresponds to the projection of the aortic arch and rises to the lower edge of the I rib at the place of its attachment to the sternum on the left.

The ventricular outlets (into the aorta and pulmonary trunk) lie at level III of the left costal cartilage, the pulmonary trunk (ostium trunci pulmonalis) - at the sternal end of this cartilage, the aorta (ostium aortae) - behind the sternum somewhat to the right.

Both ostia atrioventricularia are projected on a straight line running along the sternum from the third left to the fifth right intercostal space - the left at the left edge of the sternum, the right - behind the right half of the sternum.

Physical methods of research of the heart

Palpation of the heart region allows one to assess the position and strength of the apical impulse of the heart, its changes during dilatation and weakening of cardiac contractions, with adhesive pericarditis, left and downward displacement and intensification with severe left ventricular hypertrophy. With the help of palpation, the cardiac impulse detected during examination is specified - a concussion of the anterior chest wall during heart systole, due to significant hypertrophy of the predominantly right ventricle.

Chest percussion is used to establish the topography and size of the heart by determining the boundaries of the so-called relative cardiac dullness (corresponding to the true boundaries of S.) and the boundaries of the so-called absolute dullness, corresponding only to that part of the heart that is not covered by the lungs. The diameter of the heart and the vascular bundle is also determined.

During auscultation of the heart, the left atrioventricular valve (mitral) is heard at the apex of the heart, the right atrioventricular (tricuspid) valve is heard on the sternum on the right against the V costal cartilage.

The tone of the aortic valve is heard at the right edge of the sternum in the second intercostal space, the tone of the valve of the pulmonary trunk - in the second intercostal space at the left edge of the sternum.

Valve projections and their auscultation sites (scheme). 1 - pulmonary valve; 2 - left atrioventricular valve (mitral); 3 - right atrioventricular valve (tricuspid); 4 - aortic valve. The listening places are marked with crosses corresponding to the valves.

List of used literature

1) Borzyak E. I., Bocharov V. Ya., Volkova L. I.; / Ed. M.R.Sapina. Human anatomy. In 2 volumes. T. 2 M .: Medicine, 1986

2) Ostroverkhov G.E., Lubotsky D.N., Bomash Yu.M. Operative surgery and topographic anatomy. Moscow: Medicine 1972

3) Sinelnikov R.D. Atlas of human anatomy. In 4 volumes. - M.: Medicine, 1963

4) Human anatomy (with elements of physiology): M.R.Sapin, D. B. Nikityuk - Moscow, Medicine, 2003 - 432 p.

5) Human anatomy. Pocket guide: - St. Petersburg, AST, Astrel, 2005 - 320 s

General description of the anatomy of the chest

The chest is where the heart is located in humans, mammals and birds. It is the musculoskeletal receptacle of all organs responsible for respiration and blood circulation. Also in the chest is the esophagus and a number of large arteries and veins in the body. The chest itself is formed by the spinal column, costal arches and sternum. It communicates with other cavities and areas of the body, provides mechanical protection for the vital organs of the body.

Integral thorax and cavities

Due to the attachment of the ribs by cartilage to the sternum, the cage is formed as a closed osteochondral receptacle. Due to the intercostal muscles, external and internal fascia, as well as the musculo-tendinous diaphragm, a closed chest cavity is formed. It has several openings: the upper aperture, esophageal, aortic opening of the diaphragm, opening of the inferior vena cava. In the chest cavity itself, there are a number of vital confined spaces: the mediastinum (the place where the heart is located), the pericardial cavity, and the pleural cavities surrounding the lungs.

Projection of the heart onto the chest

The place where the human heart is located is called the mediastinum. Here is the pericardium, in which the heart is enclosed with the mouths of the main blood vessels. In this case, the heart has three boundaries, which are projected onto the chest. Their change allows you to determine deviations from the norm and specific physical symptoms of organic heart disease. Normally, the heart is located to the left of the sternum from the III intercostal space along the V intercostal space. The heart is turned slightly forward by the right ventricle. The direction of the longitudinal axis of the heart from the basal (upper) sections to the lower (apical) sections is as follows: the heart is oriented from top to bottom, back to front, right to left.

Heart borders

The right cardiac border is determined percussion and is located 1 cm to the right of the right edge of the sternum along the IV intercostal space. The left border corresponds to the apical impulse: 1.5 cm to the left of the left mid-clavicular line. The upper border, corresponding to the entire width of the vascular bundle, is located in the III intercostal space. By connecting the point of the extreme right and extreme left border with the extreme points of the width of the vascular bundle, the basic configuration of the pericardium is determined. This is the projection of the place where the human heart is.

The concept of the mediastinum

The mediastinum is the place where the human heart is located. It is a limited cavity that includes all organs located between both lungs. The anterior border of the cavity is the intrathoracic fascia and the sternum, the posterior border is the necks of the ribs, the prevertebral fascia and the thoracic spine. The lower wall is the diaphragm, and the upper wall is a collection of fascial sheets connected to the suprapleural membrane. The lateral walls of the mediastinum are sections of the parietal pleura and intrathoracic fascia. Also, for the convenience of studying the elements located here, the mediastinum is conventionally divided into upper and lower. The latter is subdivided into the posterior, central and anterior mediastinum. The place where the human heart is located is the lower central mediastinum.

Syntopy of the heart

Syntopy is a topographic concept that reflects the proximity of a certain organ with other anatomical structures. It is advisable to disassemble it together with the location of the mediastinal organs. So, the heart is not directly adjacent to any of the anatomical structures, except for the pericardium and blood vessels. But the outer pericardial leaf, which separates the organ from the rest of the anatomical structures, is just adjacent to them. In front of the pericardium are the antero-mediastinal, pre-pericardial, intrathoracic lymph nodes and vessels, surrounded by fatty tissue. Behind, the pericardium and heart are bordered by the esophagus, azygos and semi-unpaired veins, the aorta, the vagus nerve, the sympathetic trunk and the thoracic lymphatic duct.

Syntopy of the heart in the lower central mediastinum

The place where the human heart is as close as possible to the rest of the vital organs and blood vessels is called the lower central mediastinum. Here is the pericardial bag, which is two layers of the mesothelium, between which there is a small cavity. The heart itself is located behind the visceral pericardial leaf. Outside the pericardium, the roots of the lung are located: pulmonary veins and arteries, the main bronchi located below the tracheal bifurcation. There are also phrenic nerves and intrathoracic vessels with lymph nodes. Until the moment when the main vessels (aorta, vena cava, pulmonary trunk and pulmonary veins) are covered by the pericardium, they are also located in the central mediastinum. As soon as they leave the pericardial sac, they are in other parts of the mediastinum. All these features of anatomy are extremely important, because they determine the surgical tactics for chest injuries that penetrate into its cavity, and during planned operations.

Places of valve projection on the anterior chest wall.

Projection left atrioventricular (mitral) valve - to the left of the sternum in the area of attachmentIIIribs.

Projection right atrioventricular (tricuspid) valve - in the middle of the distance between the place of attachment to the sternum of the cartilageIIIleft ribs and cartilageVribs on the right.

Projection pulmonary valve - in the second intercostal space to the left of the sternum.

Projection aortic valve - in the middle of the sternum at the level of the cartilageIIIribs.

Diagram of the projection of the heart valves on the anterior chest wall (A - projection of the aortic valve; L - projection of the pulmonary valve; M - projection of the mitral valve; T - projection of the tricuspid valve) and the main points of listening to heart murmurs: 1 - apex of the heart (murmurs from the mitral valve); 2 - the second intercostal space at the right edge of the sternum (aortic valve); 3 - the second intercostal space at the left edge of the sternum (pulmonary valve); 4 - the body of the sternum above the xiphoid process (tricuspid valve); 5 - Botkin-Erb point - the fourth intercostal space to the left of the sternum (diastolic murmur of aortic insufficiency and murmurs of the mitral valve are performed); ribs are designated by roman numerals.

Listening to the heart in the places of the true projection of the valves due to their very close location from each other does not allow us to determine which of the valves is affected. The perception of sounds arising in the heart depends not only on the proximity of the valve projection, where sound vibrations occur, but also on the conduction of these vibrations along the heart muscle and blood flow. Therefore, clinical studies have established points on the chest where the sound phenomena associated with the activity of each valve are most well heard.

The point of auscultation of the mitral valve (1 point) is the area of the apical impulse, since the vibrations are well conducted by the dense muscle of the left ventricle, and the apex of the heart during systole is closest to the anterior chest wall.

Valve auscultation pointaorta (2 point) - the second intercostal space on the right at the edgesternum where the aorta comes closest to the anterior chest wall.

The point of auscultation of the pulmonary valve (point 3) is the place of the best listening coincides with its true projection, that is, it is located in the second intercostal space to the left of the sternum.

The point of auscultation of the tricuspid valve (point 4) is the lower end of the sternum at the base of the xiphoid process of the sternum(area of the right ventricle).

With insufficiency of the aortic valve, the murmur is better heard on auscultation of the point located (5 point of auscultation - Botkin-Erb point)to the left of the sternumat the attachment pointIII- IVribs.

6. Rules of auscultation of the heart.

1. The heart must be listened to in various positions: lying down, standing, after physical exertion (for example, after repeated squats).

2. It is better to listen to the heart when holding the breath after a deep inhalation and subsequent deep exhalation (so that breathing noises do not interfere). It is recommended to make commands while listening to each point: "Inhale - exhale", "hold your breath."

3. Auscultation of the heart must be performed in a strict sequence (from the 1st to the 5th point in sequence). The sound of the II tone must be compared at the 2nd and 3rd points of auscultation.

4. If any changes in the points of auscultation are detected, the entire area of the heart is carefully listened to.

3. To improve auscultation sound phenomena associated with mitral valve pathology, it is necessary to give the patient position on the left side, when the apex of the heart approaches the chest wall ; damage to the aortic valve is better detected by auscultation of the patient in an upright position with arms crossed and raised above the head and in the supine position right side.

Embolism is a blockage of blood vessels by bodies (emboli) that come with the flow of blood or lymph.

By localization, embolism of the vessels of the large, pulmonary circulation and the portal vein system is distinguished.

In all these cases, the movement of emboli mainly occurs in the direction of the natural flow of blood. It follows that the source of vascular embolism in the systemic circulation is pathological processes in the pulmonary veins, cavities of the left half of the heart, arteries of the systemic circulation, and the source of vascular embolism in the pulmonary circulation is pathological changes in the veins of the systemic circulation and the right half of the heart. The occurrence of portal vein embolism is due to pathological changes in the basin of this vein. The exception is retrograde embolism, when the movement of the embolus does not occur according to the laws of hemodynamics, but due to the gravity of the embolus itself. Such an embolism develops in large venous trunks with a slowdown in blood flow and a decrease in the suction action of the chest and right half of the heart. There is also paradoxical embolism in the case of non-closure of the atrial or interventricular septum, as a result of which emboli from the veins of the systemic circulation and the right half of the heart pass into the left, bypassing the pulmonary circulation (Fig. 24).

Embolism of exogenous etiology. Air embolism occurs after injury of large poorly collapsing veins (jugular, subclavian, dura mater sinuses), the pressure in which is close to zero or negative. This can be the cause of air embolism during medical procedures, for example, infusion of solutions into large veins. As a result, air is sucked into the veins, especially at the height of inspiration, and an embolism of the vessels of the pulmonary circulation occurs. The same conditions are created when the lung is injured or destructive processes in it, as well as during the imposition of pneumothorax, leading, however, to embolism of the vessels of the systemic circulation. Similar consequences have the flow of a large amount of air from the lungs into the blood when a person is exposed to an explosive shock wave (air, water), as well as as a result of “explosive decompression” during a rapid ascent to a considerable height. The resulting sharp expansion of the pulmonary alveoli, rupture of their walls and the flow of air into the capillaries cause inevitable embolism of the vessels of the systemic circulation.

The sensitivity of various animal and human species to air embolism is not the same. The rabbit dies after intravenous administration of 2-3 ml of air, while the dog tolerates the volume of injected air of 50-70 ml / kg. The person occupies an intermediate position.

Embolism of endogenous etiology. The cause of thromboembolism is a detached piece of blood clot. Detachment of thrombus particles is a sign of its inferiority (“sick” thrombus), caused by aseptic or purulent fusion of the thrombus, impaired thrombus retraction phase, as well as blood coagulation.

“Sick” blood clots are predominantly formed in the veins of the systemic circulation (veins of the lower extremities, pelvis, liver), which explains the high frequency of thromboembolism in the pulmonary circulation. Inflammatory changes in the valve of the pulmonary trunk and the right atrioventricular (tricuspid) valve, leading to the development of thromboendocarditis, are often accompanied by pulmonary embolism. Only when blood clots form in the left side of the heart (endocarditis, aneurysm), the aorta, or in large arteries (atherosclerosis), there is an embolism of the vessels of the systemic circulation.

Fat embolism observed when drops of fat enter the bloodstream, mainly of endogenous etiology (due to fragmentation of tubular bones, damage to subcutaneous or pelvic tissue, fatty degeneration of the liver). With age, as a result of the replacement of red bone marrow of tubular bones with yellow and an increase in the content of fats with a low melting point in it, the risk of fatty embolism increases.

Since the source of embolism is localized mainly in the basin of the veins of the systemic circulation, fat embolism develops primarily in the vessels of the pulmonary circulation. Only with time is it possible for fat droplets to penetrate through the pulmonary capillaries (or arteriovenous anastomoses of the pulmonary circulation) into the left half of the heart and arteries of the systemic circulation.

The amount of fat that can cause fatal fat embolism in various animal species ranges from 0.9 to 3 ml / kg.

Tissue (cellular) embolism. In case of injury, particles of various tissues of the body (bone marrow, muscles, brain, liver, trophoblast), especially those rich in water, can be brought into the blood circulation system, especially the pulmonary circulation. The separation of pasty fatty masses - atheroma - from the atherosclerotic arterial wall and their entry into the blood lead to embolism of the arteries of the systemic circulation.

Vascular embolism by cells (often in the form of aggregates) of malignant tumors is of particular importance, since it is the main mechanism for the formation of metastases.

Amniotic fluid embolism- the ingress of amniotic fluid during childbirth into the damaged vessels of the uterus in the area of the separated placenta. In the arterioles and capillaries of the lungs, dense particles of amniotic fluid (meconium, vemix caseosa) are retained, which is manifested by the clinical picture of pulmonary embolism. This type of embolism differs from tissue embolism by an increase in the activity of the fibrinolytic blood system, a sharp decrease in the concentration of fibrinogen in the blood (hypo- and afibrinogenemia), impaired blood coagulation (secondary) and prolonged bleeding from the uterus.

Clinical symptoms of embolism are determined by its localization (small or large circulation), features of angioarchitectonics, in particular, the state of collateral circulation and its neurohumoral regulation, the size and composition of emboli, their total mass, the rate of entry into the bloodstream, and the reactivity of the organism.

Gas embolism is the main pathogenetic link in the state of decompression, in particular, decompression sickness. The difference in atmospheric pressure from high to normal (for working caissons and divers) or from normal to sharply reduced (with a rapid rise to altitude or depressurization of the cabin of a high-altitude aircraft) causes a decrease in the solubility of gases (nitrogen, carbon dioxide, oxygen) in tissues and blood ( desaturation) and blockage by bubbles of these gases (primarily nitrogen) of the capillaries, which are localized mainly in the basin of the vessels of the systemic circulation.

Gas embolism is also possible with anaerobic (gas) gangrene.

Embolism of the vessels of the pulmonary circulation. The most important functional disorder in pulmonary embolism is a sharp decrease in blood pressure in the system of a large circle of blood circulation(fig. 25). There are several hypotheses explaining the mechanism of the hypotensive effect of pulmonary embolism.

1. Some authors associate a sharp decrease in blood pressure in the systemic circulation with a decrease in MOC due to mechanical blockage of the pulmonary artery and right ventricular failure. However, the results of further research have shown that mechanical closure of even most of the pulmonary vessels does not lead to the same disturbances as in embolism.

2. It is widely believed that a sharp drop in blood pressure is considered as reflex hypotension (Schwigka-Larin unloading reflex). It is believed that the depressive reflex is caused by irritation of receptors localized in the bed of the pulmonary artery. According to A.B. Focht and V.K. Lindemann, vagotomy, as well as atropinization of animals weaken the depressive reaction, which confirms its reflex mechanism.

3. A certain role in lowering blood pressure in pulmonary embolism is played by the weakening of heart function as a result of myocardial hypoxia, which is a consequence of an increase in the load on the right half of the heart and a sharp decrease in blood pressure.

The obligatory hemodynamic effects of vascular embolism in the pulmonary circulation include increased blood pressure in the pulmonary artery(normal systolic blood pressure in it is 20 mm Hg, diastolic - 8 mm Hg) and a sharp increase in the pressure gradient in the area of the pulmonary artery-capillaries, which is considered as a result of reflex spasm of the pulmonary vessels. Reflex narrowing of the pulmonary arterioles is necessary to keep the pressure in the pulmonary capillaries below the level at which pulmonary edema can develop.

The same effect - irritation of the receptors of the pulmonary vessels, as a result of which their spasm occurs - can lead to an increase in pressure in the pulmonary arterioles, mechanical irritation of the vessels by emboli, slowing down of blood flow in the part of the vessel located below the embolus, the release of substances at the site of blockage (serotonin, histamine, endothelin), capable of causing contraction of vascular smooth muscle fibers.

As a result of these hemodynamic disturbances, the central venous pressure rises sharply, acute pulmonary heart disease(acute right ventricular failure syndrome), which is often the cause of death.

Violation of hemodynamics in the pulmonary and systemic circulation during pulmonary embolism leads to changes in the ventilation-perfusion ratio in the lungs and, as a consequence, to secondary changes in the blood gas composition - an increase in pCO2, a decrease in pO2. Shortness of breath develops as an adaptive reaction aimed at normalizing the blood gas composition. It is believed that impaired external respiration as a result of pulmonary embolism is a reflex reaction arising both from the receptor field of the pulmonary circulation and as a result of irritation of the reflexogenic zones of the systemic circulation with blood with a low oxygen content. It has been experimentally proven that by cutting the vagus nerves, breathing disorders can be significantly reduced.

Vascular embolism in the systemic circulation. The causes of vascular embolism in the systemic circulation, as noted above, are: pathological processes (thromboendocarditis, myocardial infarction), accompanied by the formation of blood clots on the inner surface of the cavities of the left half of the heart; thrombus formation in the arteries of the systemic circulation, followed by thromboembolism; gas or fat embolism. Emboli are often localized in the coronary, middle cerebral, internal carotid, renal, splenic, and mesenteric arteries. Under other identical conditions, the localization of emboli is determined by the angle of deflection of the lateral branches of the vessel, their diameter, and the intensity of filling the organ with blood. A significant angle of deviation of the lateral branches relative to the segment of the vessel located above, their relatively large diameter, hyperemia are factors that determine the localization of emboli.

In case of gas embolism accompanying decompression sickness or “explosive decompression”, an important point in the localization of emboli in the vessels of the brain and subcutaneous fatty tissue is the high solubility of nitrogen in lipid-rich tissues.

The severity of the clinical picture is determined mainly by two factors: reflex vascular spasm and the degree of development of collaterals. Reflex spasm, on the one hand, can cover not only the nearest, but also distant vessels, complicating the course of the pathological process. In this case, local pathophysiological changes (ischemic area) are often joined by common ones, from which patients often die. On the other hand, the state of collateral circulation in the basin of a vessel blocked by an embolus and in nearby tissues is a factor that prevents such a difficult and often irreversible process as the death of the corresponding tissue site, which develops as a result of embolism.

Portal vein embolism Although it is observed much less frequently than embolism of the pulmonary and systemic circulation, it attracts attention primarily by the characteristic clinical symptom complex and extremely severe hemodynamic disorders.

Due to the large capacity of the portal bed, blockage by the embolus of the main trunk of the portal vein or its main branches leads to increased filling with blood of the abdominal organs (stomach, intestines, spleen) and the development of portal hypertension syndrome - an increase in blood pressure in the portal vein system from 0.78-0, 98 to 3.92-5.88 kPa (from 8-10 to 40-60 cm H2O). At the same time, a pathognomonic clinical triad (ascites, expansion of the superficial veins of the anterior abdominal wall, enlargement of the spleen) and other changes caused by impaired blood circulation (a decrease in blood flow to the heart, stroke volume of the heart and MOC, a decrease in blood pressure), respiration (shortness of breath, then a sharp slow breathing, apnea) and the functions of the nervous system (confusion, respiratory paralysis). The mechanism of these general disorders mainly consists in a decrease in the BCC due to the accumulation of blood (about 90%) in the portal bed. Such hemodynamic disturbances are often the direct cause of death of patients.

At the same time, there is no direct connection between ascites, the expansion of the superficial veins of the anterior abdominal wall and splenomegaly, on the one hand, and the degree of portal hypertension, on the other. Sometimes, with a high level of portal pressure, these symptoms are absent and, conversely, in some cases they occur even with a slight increase in pressure in the portal vein system. This suggests that in the development of these clinical manifestations of portal hypertension, in particular ascites, in addition to increased pressure, other factors play an important role: impaired metabolic functions of the liver; sodium and water retention in the body caused by overproduction of aldosterone and vasopressin or a violation of their destruction in the liver; decrease in oncotic blood plasma pressure due to hypoproteinemia; increasing the permeability of the capillaries of the portal bed.