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How It Works & Images

The heart receives its own supply of blood from the coronary arteries. Two major coronary arteries branch off from the aorta near the point where the aorta and the left ventricle meet. These arteries and their branches supply all parts of the heart muscle with blood.

Left Main Coronary Artery (also called the left main trunk)

The left main coronary artery branches into:

  • Circumflex artery
  • Left Anterior Descending artery (LAD)

The left coronary arteries supply:

  • Circumflex artery – supplies blood to the left atrium, side and back of the left ventricle
  • Left Anterior Descending artery (LAD) – supplies the front and bottom of the left ventricle and the front of the septum

Right Coronary Artery (RCA)

The right coronary artery branches into:

  • Right marginal artery
  • Posterior descending artery

The right coronary artery supplies:

  • Right atrium
  • Right ventricle
  • Bottom portion of both ventricles and back of the septum

The main portion of the right coronary artery provides blood to the right side of the heart, which pumps blood to the lungs. The rest of the right coronary artery and its main branch, the posterior descending artery, together with the branches of the circumflex artery, run across the surface of the heart’s underside, supplying the bottom portion of the left ventricle and back of the septum.

What is collateral circulation?

Collateral circulation is a network of tiny blood vessels, and, under normal conditions, not open. When the coronary arteries narrow to the point that blood flow to the heart muscle is limited (coronary artery disease), collateral vessels may enlarge and become active. This allows blood to flow around the blocked artery to another artery nearby or to the same artery past the blockage, protecting the heart tissue from injury.

Collateral vessels surround blocked blood vessel

Cardiac anatomy revisited

J Anat. 2004 Sep; 205(3): 159–177.

Robert H Anderson

1Institute of Child Health, University College, London, UK

Reza Razavi

1Institute of Child Health, University College, London, UK

2Guy’s and St Thomas’s Hospitals, London, UK

Andrew M Taylor

1Institute of Child Health, University College, London, UK

1Institute of Child Health, University College, London, UK

2Guy’s and St Thomas’s Hospitals, London, UK

Correspondence Professor Robert H. Anderson, Cardiac Unit, Institute of Child Health, 30 Guilford Street, London WC1H 1EJ, UK. E: [email protected] © Anatomical Society of Great Britain and Ireland 2004This article has been cited by other articles in PMC.

Abstract

In tomorrow’s world of clinical medicine, students will increasingly be confronted by anatomic displays reconstructed from tomographically derived images. These images all display the structure of the various organs in anatomical orientation, this being determined in time-honoured fashion by describing the individual in the ‘anatomical position’, standing upright and facing the observer. It follows from this approach that all adjectives used to describe the organs should be related to the three orthogonal planes of the body. Unfortunately, at present this convention is not followed for the heart, even though most students are taught that the so-called ‘right chambers’ are, in reality, in front of their ‘left’ counterparts. Rigorous analysis of the tomographic images already available, along with comparison with dissected hearts displayed in attitudinally correct orientation, calls into question this continuing tendency to describe the heart in terms of its own orthogonal axes, but with the organ positioned on its apex, so that the chambers can artefactually be visualized with the right atrium and right ventricle in right-sided position. Although adequate for describing functional aspects, such as ‘right-to-left’ shunting across intracardiac communications, this convention falls short when used to describe the position of the artery that supplies the diaphragmatic surface of the heart. Currently known as the ‘posterior descending artery’, in reality it is positioned inferiorly, and its blockage produces inferior myocardial infarction. In this review, we extend the concept of describing cardiac structure in attitudinally correct orientation, showing also how access to tomographic images clarifies many aspects of cardiac structure previously considered mysterious and arcane. We use images prepared using new techniques such as magnetic resonance imaging and computerized tomography, and compare them with dissection of the heart made in time-honoured fashion, along with cartoons to illustrate contentious topics. We argue that there is much to gain by describing the components of the heart as seen in the anatomical position, along with all other organs and structures in the body. We recognize, nonetheless, that such changes will take many years to be put into practice, if at all.

Keywords: anatomical position, attitudinally correct orientation, cardiac septal structures, computerized tomography, magnetic resonance imaging

Introduction

One of the major conventions of human anatomy is that all structures within the body should be described in the setting of the anatomical position. Thus, the locations of structures within organs, or the relations of organs to each other, are described on the basis of the subject standing upright, and facing the observer. This principle has withstood well the passage of time, and has permitted surgeons and physicians accurately to describe the various symptoms of disease, and to establish the best options for treatment. Perhaps surprisingly, anatomists over the years have uniformly failed to observe this convention when describing the human heart. Internal cardiac structure has consistently, and inappropriately, been considered in the setting of the heart positioned on its apex, with the atriums above the ventricles – the so-called ‘Valentine’ approach, reflecting the convention of illustrating the organ in characteristic shape balanced on its apex for the greetings cards issued to lovers celebrating St Valentine’s Day.

In the days when diagnosis was largely achieved by inspection or auscultation, and when treatment was by medicines or surgical, this deviation from standard anatomical practice was of little consequence. Indeed, it had some advantages, because most recognized that the so-called ‘right’ chambers were in reality anterior to the ‘left’ counterparts, and this preserved the reality of describing ‘left-to-right’ or ‘right-to-left’ shunting in the presence in intracardiac communications. It was somewhat confusing, nonetheless, for the beginner to be told that blockage of the allegedly ‘posterior’ descending coronary artery produced inferior myocardial infarction. Nowadays, the departure from the accepted norm has much more significant consequences. This is because, increasingly, the cardiologist treats structural problems within the heart by means of interventional catheterization. It is then very confusing for the trainee, observing the operator advance a catheter from the groin through the inferior caval vein into the heart, to be told that the catheter is moving ‘anteriorly’ when, in reality, it can be seen moving upwards in the fluoroscopic screen, in which the image of the patient is still shown in the anatomical position. From the stance of the electrophysiologist, this deficiency has now been addressed by a group of European and North American experts, which recommended that the cardiac components be described as seen in the anatomical position (Cosio et al. 1999). The methods used for diagnosis now also facilitate this approach, as images are increasingly obtained using magnetic resonance or computed tomography, techniques that visualize not only the heart, but also the surrounding thoracic structures. In addition to setting the scene for appropriate anatomical description, these new techniques provide the sophistication to reveal cardiac anatomy in its smallest details, clarifying many previously confusing topics such as the arrangement of the cardiac septal structures (Anderson et al. 1999), and the nature of attachment of the leaflets of the arterial valves (Anderson, 2000). If the fullest advantage is to be gained from describing cardiac structure in appropriate fashion (Cook & Anderson, 2002), it is important that students be introduced to the correct arrangement during their initial introduction to human anatomy. In this review, therefore, we describe the structure of the heart as it lies within the body as revealed with clinical tomographic images, correlating the findings where necessary with standard anatomical dissections.

The location of the heart within the thorax

As demonstrated by the chest radiograph viewed in the frontal projections (), the heart is usually positioned within the mediastinum with one-third of its mass to the right of the midline, and with its own long axis directed from the right shoulder towards the left hypochondrium. There are variations in this cardiac position from patient to patient according to bodily make-up or disease, and minor changes occur with respiration. In very rare circumstances, the entire bodily structure can be mirror-imaged in the setting of normality, or when there is an associated congenital cardiac malformation. In other circumstances, more common than the mirror-imaged situation, but still relatively rare, the structures of the body that usually demonstrate lateralization are arranged in isomeric fashion (Anderson et al. 1998). For the purposes of this review, nonetheless, we will confine ourselves to the usual situation, often described as ‘situs solitus’.

The frontal chest radiograph (a) shows the outline of the cardiac silhouette relative to the thorax. Note that the axes of the heart itself are well out of skew relative to the axes of the body. The right border of the heart is shown by the red dotted line, the left border, or obtuse border of the ventricular mass, by the yellow dotted line, and the diaphragmatic border, or acute border of the ventricular mass, by the green dashed line. A cast of the normal heart (b), photographed in attitudinally appropriate position, with the so-called ‘right heart’ cast in blue, and the ‘left heart’ cast in red, shows the chambers corresponding to the silhouette. See also .

With the advent of tomographic imaging, which, subsequent to the acquisition of the data set containing the cardiac images, permits the structure of the heart to be displayed in any desired plane, it is possible accurately to show the structures that produce the borders of the frontal cardiac silhouette as revealed in the chest radiograph. Such frontal sections show that the right border of the silhouette, more or less vertical, is produced by the right atrium, with the caval veins entering at its top and bottom (, middle; compare with ). The inferior border is made by the right ventricle, extending horizontally along the diaphragm to the cardiac apex, with the left border sloping upwards from the apex and formed by the wall of the left ventricle (, left). At the top of the left border, a small part of the left atrium, specifically its appendage, contributes to the silhouette (, right). The pulmonary trunk and aorta then emerge from the superior border of the silhouette, with the aorta in rightward position ().

The cuts through the heart in the coronal plane, running from the front (a) to the back (c), show the different chambers that contribute to the borders of the cardiac silhouette as seen in the frontal chest radiograph (). See text for further discussion.

With the advances made in manipulation of the data set containing the resonance images, we are now able to reconstruct the various chambers and their components and superimpose them on the silhouette. In this way, we can accurately position the cardiac valves within the frontal section, showing that the pulmonary valve is positioned superiorly and the tricuspid valve inferiorly (), these two valves of the so-called ‘right heart’ being separated one from the other, and positioned in front of their counterparts in the ‘left heart’ (). The two valves of the left heart are directly adjacent one to the other, with the fibrous continuity between them forming the roof of the left ventricle (). As already stated, the leaflets of the pulmonary and tricuspid valves are widely separated in the roof of the right ventricle, with the leaflets of the pulmonary valve lifted away from the base of the ventricular mass on the free-standing sleeve of the subpulmonary muscular infundibulum (). The reconstructions also show that, whereas the leaflets of the mitral and tricuspid valves are hinged from the atrioventricular junctions in relatively planar fashion, those of the arterial valves are attached in semilunar form, being suspended from the circular sinutubular junctions (). These sinutubular junctions of the aortic and pulmonary valves themselves have a marked obliquity relative to each (), with the intrapericardial components of the arterial trunks then spiralling round one another as they extend from the base of the ventricular mass into the mediastinum ().

The outlines of the cardiac valvar leaflets from the data set shown in have been reconstructed in the frontal plane (a) and superimposed on the chest radiograph (b).

The outlines of the cardiac valves reconstructed from the magnetic resonance images are shown in lateral projection, and compared with the short axis of the heart as seen in left anterior oblique projection looking upwards from the cardiac apex. The green dotted line shows the fibrous continuity between the leaflets of the aortic and mitral valves that forms the roof of the left ventricle. Note that, in comparison, the roof of the right ventricle is muscular, the supraventricular crest (red arrow) being interposed between the leaflets of the tricuspid and pulmonary valves.

The short axis of the heart is photographed from above and behind having removed the atrial chambers and the arterial trunks. Note the obliquity of the relationship between the aortic and pulmonary valves, and that the pulmonary trunk is lifted away from the ventricular base by the subpulmonary muscular infundibulum. See also .

The upper panel shows the opened pulmonary root having removed the leaflets of the pulmonary valve. The semilunar attachments of the leaflets are marked by the red line, with the blue line showing the sinutubular junction, the yellow line the anatomic junction between the muscular infundibulum and the arterial wall of the pulmonary trunk, and the green line the ring made by joining together the basal attachments of the three arterial valvar leaflets. The lower panel shows the three-dimensional crown-like configuration produced by interdigitation of the semilunar attachments with the three rings existing in the root. There is no ‘annulus’ supporting the attachments of the leaflets – see text for further discussion.

The ventricles and arterial trunks have been reconstructed from a data set obtained using magnetic resonance imaging, and the so-called right-sided structures coloured in blue, with the left-sided structures coloured in red. Note the spiralling arrangements of the arterial trunks. The apparent hole in the cast of the right ventricle is produced by the prominent right ventricular trabeculations.

Location of the chambers within the heart

The software now available permits the contours of the separate cardiac chambers to be reconstructed and displayed within the setting of the thorax. Such reconstructions confirm that the so-called ‘right’ chambers are anterior to their ‘left-sided’ counterparts and, equally importantly, that the atrial chambers are positioned to the right of their respective ventricles. The heart itself is positioned with its own axes obliquely orientated relative to the body, so that a sagittal section through the thorax taken in the midline shows the right ventricle positioned most anteriorly, with the left atrium posteriorly located (). Cardiologists are today also able to obtain three-dimensional reconstructions of cardiac structure by means of an ultrasonic scanner introduced through the oesophagus and into the stomach. The sagittal scans show well the potential access of the ultrasonic beam from the oesophagus into the various cardiac components ().

The magnetic resonance image, taken in lateral projection (sagittal plane), shows that the so-called right-sided structures, the right ventricle, infundibulum and pulmonary trunk, are in reality anterior to their left-sided counterparts.

A slice parallel to the image shown in reveals the location of the oesophagus directly posterior to the so-called left-sided cardiac structures.

Sectioning the heart in its own short axis then shows the rationale underlying the traditional description of the margins of the cardiac silhouette as seen in the chest radiograph (). Sections taken across the ventricular mass reveal that the cone of ventricular musculature is squashed, so that the inferior border lies along the diaphragm (). The ventricular septum transects this inferior margin. The squashing of the cone produces a triangular configuration, with the other two sides of the triangle being adjacent to the sternocostal border anteriorly and to the right, and being located within the cardiac notch of the left lung posteriorly and to the left. The particular shape of the triangle is such that the angle made at the anterior margin between the sternocostal and diaphragmatic surfaces, and the angle between the pulmonary and diaphragmatic borders posteriorly, are both acute, being less than 90°. The angle at the superior margin, by contrast, between the sternocostal and pulmonary surfaces, is obtuse, being greater than 90°. Hence, the inferior margin of the cardiac silhouette, representing the anterior border, is known as the acute margin, and corresponds to the site of the acute marginal branch of the right coronary artery. The leftward border as seen in the chest radiograph, representing the superior margin of the ventricular cone, is described as the obtuse margin, with the obtuse marginal branches of the circumflex artery irrigating the pulmonary surface of the ventricular mass ().

The section across the ventricular mass in short axis shows that the angle between the sternocostal and diaphragmatic surfaces is acute, giving the acute margin, whereas that between the sternocostal and pulmonary margins is obtuse. It also shows how the short axis of the left ventricle can be divided into quadrants (red lines). Quadrant 4 is obviously positioned inferiorly. Currently, however, nuclear cardiologists describe the opposite quadrant (2) as being ‘anterior’. As the images show, this quadrant is really positioned superiorly. It is the septal quadrant (1) that is anterior.

The magnetic resonance images have been programmed to permit the data set to be cut in the plane of the coronary arteries. The section shows the obtuse marginal branches of the circumflex artery irrigating the obtuse margin of the ventricular mass, with the right coronary artery taking its acute turn at the acute margin (star).

Another important cardiac landmark is found on the diaphragmatic surface of the heart, at the point at which the ventricular septum transects the inferior border. It is found at the site where the plane of the septal structures crosses the plane of the inferior atrioventricular groove (). Known as the ‘crux’, this landmark is particularly important for the echocardiographer, because a section taken parallel but superiorly to the diaphragmatic surface reveals all four cardiac chambers, hence its description as the ‘four-chamber’ plane (). From what has been described thus far, it is evident that, owing to the obliquity of the cardiac axes relative to the bodily axes, this ‘four-chamber’ plane cannot be obtained by taking standard sagittal or coronal sections through the body. The echocardiographer therefore has to obtain images of the heart through the various echocardiographic ‘windows’ (Anderson et al. 2001), with the transoesophageal portal now becoming increasingly important ().

The section across the ventricular mass in its own short axis shows how the postero-inferior extent of the ventricular septum (red star) cuts the atrioventricular junction between the right (RAVO) and left (LAVO) atrioventricular orifices. This corresponds to the so-called crux of the heart (see also ). Note how the atrial myocardium (green dotted line) overlaps the ventricular myocardium at this point, the two muscle masses separated by the fibro-fatty tissue of the atrioventricular groove.

The long axis taken along the heart itself shows the so-called ‘four-chamber’ projection.

Examination of the cross-section of the ventricular mass then reveals the fundamental nature of the problem currently existing in the accepted description of cardiac structures. The artery that irrigates the inferior part of the ventricular septum (), and the adjacent inferior ventricular walls, is currently described as the ‘posterior descending artery’. As shown unequivocally by the resonance images, this artery is located inferiorly rather than posteriorly. As already emphasized, blockage of the artery is known to produce inferior ventricular infarction (Cook & Anderson, 2002). The description of the electrocardiographic recordings remains appropriate because these are automatically registered relative to the anatomical position. Problems now exist, however, with the way that nuclear cardiologists have agreed to describe the various quadrants of the ventricular mass. Until recently, the quadrant adjacent to the diaphragm was considered to be posterior, when self-evidently it is inferior. This solecism was corrected by the task force assembled by nuclear cardiologists and radiologists, which recognized the inferior location of this quadrant (American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging, 2002). For reasons that are not clear, however, the writing group continued to suggest that the opposite quadrant should be described as being ‘anterior’. The antonym of ‘inferior’, of course, is ‘superior’ and not ‘anterior’. Examination of the resonance images shows unequivocally that it is the septal quadrant of the left ventricular cone that is anterior, while the posterior quadrant is the one closest to the spine. The other two quadrants therefore are located inferiorly and superiorly ().

The artery that irrigates the superior quadrant of the ventricular mass, currently described as being ‘anterior descending’, is one of the major branches of the left coronary artery (). Blockage of the artery is currently described as producing antero-septal infarction. As shown by the tomographic images (), it would be much more accurate to re-name this artery as the antero-superior interventricular artery, although it is likely to continue to be known simply as the ‘ADA’.

The magnetic resonance image in frontal projection shows that the so-called ‘anterior descending coronary artery’ emerges from the aorta in superior position.

Relationships of the components of the cardiac chambers

The resonance images, when reconstructed, reveal particularly clearly the arrangement of the different cardiac chambers, showing various features that are currently ignored in standard descriptions.

The atrial chambers each possess a body, a venous component, a vestibule and an appendage. The two chambers are separated one from the other by the septum. The body of the right atrium is virtually non-existent, although clearly evident in fetal sections (). It is the space that separates the leftward boundary of the systemic venous sinus from the septum. It is difficult, if not impossible, to recognize this part in the definitive postnatal heart, because the left venous valve is usually fused with the septal surface after birth. It is possible, nonetheless, to recognize the extensive appendage, with its pectinated wall, the smooth-walled vestibule supporting the hingelines of the tricuspid valve, and the extensive venous sinus into which drain the superior and inferior caval veins along with the coronary sinus (). The junction between the appendage and the systemic venous sinus is marked internally by the extensive and prominent terminal crest (‘crista terminalis’), with this corresponding externally with the terminal groove (‘sulcus terminalis’). The remnants of the right venous valve, the Eustachian and Thebesian valves, are attached to this crest, with the pectinate muscles extending in parallel fashion from the crest to run all round the vestibule, separating the smooth-walled venous sinus from the smooth-walled vestibule.

This section of a developing human heart at Carnegie stage 15, and taken in ‘four-chamber’ projection, shows that, at early stages, the systemic venous sinus is separated from the remainder of the developing right atrium by well-formed right and left venous valves.

The cast of the right atrium, photographed in lateral projection from the right side, shows how the pectinated appendage interposes between the smooth-walled systemic venous sinus, receiving the superior and inferior caval veins (SCV, ICV) and the coronary sinus, and the vestibule of the tricuspid valve.

The left atrium has an obvious smooth-walled body, interposed between the vestibular and pulmonary venous components, with the pulmonary veins at the four corners of the venous part enclosing a prominent atrial dome (). Reconstructions from the tomographic images now demonstrate the precise relationships of the great veins to each other and to both atrial chambers (), with detailed analysis now revealing unexpected variations within the normal arrangement (Kato et al. 2003; Lickfett et al. 2004). The appendage of the left atrium is a true diverticulum, with all the pectinated muscles contained within it, so that the larger part of the internal surface of this atrium is smooth-walled. There is no muscular structure comparable to the terminal crest to be found in the left atrium ().

The cast of the left atrium shows that the pectinate muscles are confined within the tubular appendage, but an extensive smooth-walled body interposes between the vestibule of the mitral valve and the pulmonary venous component.

Reconstruction from magnetic resonance images showing the interrelations of the systemic and pulmonary venous components from (a) the front and (b) the back.

This cut in the short axis of the heart itself shows the triangular right atrial appendage (white star), with a broad junction to the atrium (double-headed arrow), marked by the prominent terminal crest (red star). In comparison, the junction of the left atrial appendage with the atrium is narrow, and is not marked by any terminal crest.

The coronary sinus drains to the systemic venous sinus of the right atrium. Morphologically, it is related to the left atrium, running within the left atrioventricular groove (). Within this groove, it possesses it own muscular walls (Chauvin et al. 2002), there being no evidence to support the notion that a ‘party wall’, allegedly derived from a purported left sinuatrial fold, is interposed between the cavities of the coronary sinus and left atrium (Knauth et al. 2002). When there is a persistent left superior caval vein, it almost always drains to the coronary sinus, having coursed between the left appendage and the left pulmonary veins. This arrangement is found in about one-twentieth of individuals with congenital cardiac malformations, but more usually this left-sided embryonic channel regresses, being represented in the postnatal heart by the oblique vein of the left atrium ().

The cast of the cardiac chambers, photographed to show the diaphragmatic aspect, shows how the coronary sinus occupies the left atrioventricular groove, receiving the great cardiac vein at its origin at the site of the oblique vein of the left atrium, and the middle cardiac vein at the crux.

Until recently, it was usual to see the ventricles described as possessing a ‘sinus’ and a ‘conus’. It is difficult to find evidence of any anatomical boundaries that support this convention, although examination of congenitally malformed hearts shows that it is more logical to analyse the ventricular chambers as possessing three components (Anderson & Ho, 1998). This is because the ventricles are the pumps to the circulations, and efficient pumps possess inlet and outlet valves, along with a driving piston. So do the ventricles. When analysing in this fashion, we recognize that the ventricular mass extends from the atrioventricular to the ventriculo-arterial junctions. The inlet components then surround and support the atrioventricular valves, along with their tension apparatus. The apical components are the most characteristic intrinsic components of the ventricles, with the apex of the right ventricle, situated anteriorly, being coarsely trabeculated in comparison with the fine criss-crossing trabeculations found in the posterior left ventricular apex (). The inlets also differ markedly in the normal ventricles, as do the outlets. Thus, the tricuspid valve, possessing inferior, septal and antero-superior leaflets, has extensive cordal attachments to the ventricular septum, and is supported by markedly eccentric papillary muscles. The mitral valve possesses only two leaflets, located anteriorly and posteriorly but positioned obliquely within the left ventricle, and closing along a solitary zone of apposition (). Significantly, this solitary zone of apposition is orientated in concavo-convex fashion, with the leaflets guarding markedly dissimilar proportions of the valvar circumference (). Because of this, it is usual to find slits in the extensive posterior leaflet, hinged from the parietal part of the atrioventricular junction, and guarding two-thirds of the valvar orifice. The anterior leaflet is much deeper, but guards only one-third of the orifice. This leaflet is separated from the septum by the subaortic vestibule, having fibrous continuity with two of the leaflets of the aortic valve (). Because of the obliquity of the valve within the left ventricle, it is better to describe the two leaflets as being mural and aortic, a concept that dates back to Andreas Vesalius and the birth of observation-based anatomy in Padova in the 16th century. The papillary muscles of the valve are also distinctive, being paired and positioned one at each end of the solitary zone of apposition between the valvar leaflets. Tendinous cords attach each muscle to both leaflets. Currently, the muscles are described by clinicians as being ‘postero-septal’ and ‘antero-lateral’. The difference in antero-posterior disposition, however, is marginal. As shown by either tomographic images () or cross-sectional echocardiograms, the muscles are positioned infero-septally and supero-laterally. Only time and consensus will determine the most appropriate names for these papillary muscles.

The heart has been sectioned in its own long axis to reveal the four cardiac chambers (compare with ). Note the coarse trabeculations at the apex of the right ventricle in comparison with the smooth surface of the left ventricle.

The mitral valve is photographed from above to show its atrial aspect in closed position. The two leaflets close along a solitary zone of apposition, with multiple slits in the larger leaflet ensuring competent coaptation. Original photograph reproduced by kind permission of Dr Val S. Galstyan, Armenia.

The magnetic resonance images in frontal (a) and short axis (b) planes across the body show that the paired papillary muscles supporting the mitral valves are positioned adjacent to the septum and inferiorly (yellow star with red line), and posteriorly and superiorly (red star with yellow line).

The arrangement of the tendinous cords has also been a matter of controversy. Although some have devised complex systems to categorize the cords supporting the leaflets (Silver et al. 1971), in our opinion it is sufficient to distinguish those attached to the free-edge from those attached to the ventricular surface of the leaflets, these latter being either the strut or basal cords. The most important feature, particularly for the mitral valve, is that tendinous cords should support the entirety of the free edges of both leaflets (). Unequal support to the free edge is believed to be the mechanism leading to prolapse of the leaflets (Van der Bel-Kahn et al. 1985).

The two leaflets of the mitral valve, both supported all along their free edge by tendinous cords, guard markedly dissimilar lengths of the valvar orifice, the mural leaflet (red) being long and shallow whereas the aortic leaflet (blue) is short and deep.

Important differences are also found in the structure of the ventricular outlets. In the right ventricle, the anteriorly located pulmonary valve is lifted in its entirety away from the ventricular base by the extensive free-standing infundibular sleeve (). When seen internally, the arrangement produces an extensive muscular shelf between the hinges of the tricuspid and pulmonary valves, the so-called supraventricular crest (‘crista supraventricularis’–). On the septal aspect, this crest inserts between the limbs of another important right ventricular landmark, namely the septomarginal trabeculation, or septal band (). This muscular strap reinforces the septal surface of the right ventricle, breaking up at the apex to form the moderator band and the anterior papillary muscle, and giving rise to a further series of septoparietal trabeculations that run to the parietal ventricular wall. These structures are absent from the left ventricle, where the outlet is much reduced in size because of the fibrous continuity between two of the leaflets of the aortic valve and the aortic leaflet of the mitral valve.

The photograph of the septal aspect of the right ventricle shows the arrangement of the muscle bundles, with the supraventricular crest inserting between the limbs of the septomarginal trabeculation. The septomarginal trabeculation has a body (blue star) and superior (red star) and inferior (yellow star) limbs, the two limbs clasping the insertion of the supraventricular crest (yellow dotted line). The medial papillary muscle arises from the inferior limb. Note also the septoparietal trabeculations and the moderator band.

Although the two ventricular outlets have important differences in their structure, they also have one feature in common, namely the semilunar attachment of their leaflets. This is the more significant, because surgeons continue to describe these valves as possessing an ‘annulus’. There are, in fact, at least three rings to be found within the ventricular outlets, but none supports the hingelines of the valvar leaflets. The rings are the sinutubular junction distally, the anatomic ventriculo-arterial junction within the valvar complex, and a virtual ring proximally, the last constructed by joining together the nadir of the semilunar hinges of the three leaflets (). The discrepancy between the anatomic and haemodynamic ventriculo-arterial junctions, the latter represented by the semilunar hingelines of the leaflets, has important consequences for the relationships of the outflow tracts that can now be revealed by the tomographic images.

Because the semilunar attachments extend from within the ventricles to the sinutubular junctions, they cross the circular anatomic ventriculo-arterial junctions where the musculature of the ventricles supports the fibro-elastic walls of the arterial trunks. This arrangement is best seen in the right ventricle, where all the valvar leaflets are supported by the muscular infundibulum (). The base of each leaflet is supported by muscle proximal to the anatomic junction, while the triangles between the distal attachments of the leaflets are made of fibrous tissue, and separate the ventricular outflow tract from the pericardial cavity. The same arrangement is then found in the left ventricular outflow tract, with the fibrous interleaflet triangles immediately beneath the sinutubular junction separating the left ventricular cavity from the pericardial cavity (), and also from the tissue plane existing between the back of the subpulmonary infundibulum and the aortic root (Anderson, 2000).

The magnetic resonance image (upper) and anatomic section (lower) show the relationships produced because of attachment of the leaflets of the aortic valve at the sinutubular junction. Because of the height of this attachment (red arrows), a fibrous extension of the aortic root separates the outflow tract from the transverse sinus of the periciardium (yellow double-headed arrow). The blue arrow shows the attachment of the wall of the right atrium.

The triangle formed between the non-coronary and right coronary leaflets of the aortic valve is of particular interest because, at its base, this area is continuous with the membranous septum. The fibrous triangle interposes between the left ventricular outflow tract and the right side of the transverse sinus of the pericardium (). How can such a fibrous membrane, part of the septal components of the heart, also be a parietal structure? The answer is simple. Initially, this part of the developing heart was encased in a muscular sleeve that extended to the sinutubular junction (Ya et al. 1998). Subsequent to formation and maturation of the arterial valvar sinuses and leaflets, the muscular sleeve regresses to the level of the anatomic ventriculo-arterial junction. This process then leaves the fibrous walls of the outflow tract interposed between the ventricular cavities and extracardiac space ().

Structure of the septal components

The tomographic images also serve to clarify the arrangement of those parts of the heart that are directly interposed between adjacent chambers, rather than being parietal walls. This is the definition we have suggested to distinguish between partitions that separate directly adjacent chambers, as opposed to folds that interpose between chambers but incorporate within them extracardiac tissues (Anderson & Brown, 1996).

The tomographic images show exquisitely how the so-called ‘septum secundum’, forming the superior, anterior and posterior rims of the oval fossa, is no more than an infolding of the atrial walls, at its deepest between the attachments of the pulmonary veins to the left atrium and the caval veins to the right (). The true atrial septum is the flap valve of the oval foramen, along with the antero-inferior buttress that anchors the flap to the atrioventricular junctions (Anderson et al. 1999). Significantly, the tomographic images then clarify the arrangement of the atrial and ventricular musculatures in the floor of the triangle of Koch. Initially, we thought that this important area, which contains the atrial components of the atrioventricular conduction axis, was a muscular atrioventricular septum (Becker & Anderson, 1982). We have now come to appreciate that, in reality, the area is a muscular sandwich, with an extension from the inferior atrioventricular groove interposed between the myocardial layers (). The true atrioventricular septum is that part of the membranous septum positioned on the atrial aspect of the hinge of the septal leaflet of the tricuspid valve. The remainder of the membranous septum is positioned between the cavities of the two ventricles (), and is continuous superiorly with the fibrous triangle that separates the attachments of the non-coronary and right coronary leaflets of the aortic valve at the level of the sinutubular junction ().

The long axis (oblique axial) image across the atrial chambers shows the structure of the atrial septum. Note that the septum itself is directly related to the aorta. The yellow double-headed arrow is through the floor of the oval fossa. The supero-posterior rim of the fossa, however, often described as the ‘septum secundum’, is shown by the image to be a deep infolding between the connections of the pulmonary veins to the left atrium and the caval veins to the right atrium. This area is better described as the interatrial groove (green and red arrow).

The section through the aortic root shows the relationships of the membranous part of the septum. The hingepoint of the tricuspid valve, emphasized by the blue dotted line, divided the fibrous part of the septum into atrioventricular (red arrow) and interventricular (yellow arrow) components.

As already discussed, the images also confirm that the subpulmonary infundibulum, inserting between the limbs of the septomarginal trabeculation, is for its most part a free-standing sleeve. Only a very small part of this structure is positioned as a true septum between the subpulmonary and subaortic outflow tracts. The larger part of the extensive muscular ventricular septum separates the apical ventricular components. Also significant is the fact that, because of the deeply wedged location of the subaortic outflow tract within the left ventricle, most of the septum beneath the septal leaflet of the tricuspid valve separates the right ventricular inlet from the subaortic outlet ().

This frontal section, through the part of the muscular septum that supports the membranous septum (yellow arrow) and the aortic root, shows that the muscular septum itself, by virtue of the deeply ‘wedged’ location of the left ventricular outflow tract, separates the inlet of the right ventricle from the subaortic outlet of the left ventricle (green and red arrow). Previously, we had considered this part of the septum to be an ‘inlet septum’. In reality, it is an ‘inlet–outlet’ septum.

Conclusions

There are many important aspects of cardiac anatomy that we have ignored in our review, such as the arrangement and disposition of the coronary arteries. The sophistication of tomographic imaging is now such that these features can also be demonstrated with great precision, making it possible to identify the site of any atherosclerotic lesions that might cause ischaemic myocardial disease (). Such investigations have great potential for preventive medicine. Interpretation of these, and all other images, will be greatly enhanced in future if students learn cardiac anatomy, as with the anatomy of all other organs, in the setting of the anatomical position. It is easy to understand why, in the past, morphologists and anatomists removed the heart from the body, and described its parts in isolation. There is now no reason to continue to use a system of anatomical description based on this approach, even if its usage will remain in such matters as the description of the direction of shunting of blood between the cardiac components. If we are to rationalize nomenclature, however, this can only be done by consensus, and by demonstration that the new system is better than the one it is intended to replace. The advent of the new techniques for imaging, such as resonance imaging, computerized tomography and three-dimensional echocardiography, all display cardiac structure in its appropriate bodily context. This therefore needs to be the context for a logical revision of anatomic terminology for the heart. It might be argued that, from the stance of the interventional cardiologist, the heart is a ‘stand-alone’ organ. The experiences of electrophysiologists, however, have demonstrated that this is not the case, because the catheters are manoeuvred into the heart using the standard anatomical coordinates (Cosio et al. 1999). The tomographic images also serve to clarify some of the more difficult areas of cardiac morphology, such as the arrangement of the septal structures, and the three-dimensional structure and relationships of the arterial roots. Our review, we hope, has demonstrated the advantage of the anatomist keeping abreast of these remarkable achievements in imaging.

Computed tomography section through the right coronary artery shows the potential for the new imaging techniques. The image, expanded in the inset, has revealed the presence of a calcified, atherosclerotic plaque (white arrows, black arrow shows calcification), significantly reducing the calibre of the vessels, and potentially producing myocardial ischaemia. Reproduced by kind permission of Dr Ronald Kuzo, MD (Mayo Clinic, Jacksonville, FL, USA), and Professor Jan Bogaert, MD, PhD (Gasthuisberg University Hospital, Leuven, Belgium).

Acknowledgments

The research on which this review is based was supported by grants from the British Heart Foundation together with the Joseph Levy Foundation. Research at the Institute of Child Health and Great Ormond Street Hospital for Children NHS Trust benefits from R & D funding received from the NHS Executive. We are also indebted to our colleagues in the United States of America and Belgium for permission to reproduce .

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Anatomy of the heart and blood vessels

What are the heart and blood vessels?

Blood vessels form the living system of tubes that carry blood both to and from the heart. All cells in the body need oxygen and the vital nutrients found in blood. Without oxygen and these nutrients, the cells will die. The heart helps to provide oxygen and nutrients to the body’s tissues and organs by ensuring a rich supply of blood.

Not only do blood vessels carry oxygen and nutrients, they also transport carbon dioxide and waste products away from our cells. Carbon dioxide is passed out of the body by the lungs; most of the other waste products are disposed of by the kidneys. Blood also transports heat around your body.

Where are the heart and blood vessels found?

The heart is a fist-sized organ which lies within the chest behind the breastbone (sternum). The heart sits on the main muscle of breathing (the diaphragm), which is found beneath the lungs. The heart is considered to have two ‘sides’ – the right side and the left side.

The heart has four chambers – an atrium and a ventricle on each side. The atria are both supplied by large blood vessels that bring blood to the heart (see below for more details). Atria have special valves that open into the ventricles. The ventricles also have valves but, in this case, they open into blood vessels. The walls of the heart chambers are made mainly of special heart muscle. The different sections of the heart have to squeeze (contract) in the correct order for the heart to pump blood efficiently with each heartbeat.

What do the heart and blood vessels do?

The heart’s main function is to pump blood around the body. Blood carries nutrients and waste products and is vital to life. One of the essential nutrients found in blood is oxygen.

The right side of the heart receives blood lacking oxygen (deoxygenated blood) from the body. After passing through the right atrium and right ventricle this blood is pumped to the lungs. Here blood picks up oxygen and loses another gas called carbon dioxide. Once through the lungs, the blood flows back to the left atrium. It then passes into the left ventricle and is pumped into the main artery (aorta) supplying the body. Oxygenated blood is then carried though blood vessels to all the body’s tissues. Here oxygen and other nutrients pass into the cells where they are used to perform the body’s essential functions.

A blood vessel’s main function is to transport blood around the body. Blood vessels also play a role in controlling your blood pressure.

Blood vessels are found throughout the body. There are five main types of blood vessels: arteries, arterioles, capillaries, venules and veins.

Arteries carry blood away from the heart to other organs. They can vary in size. The largest arteries have special elastic fibres in their walls. This helps to complement the work of the heart, by squeezing blood along when heart muscle relaxes. Arteries also respond to signals from our nervous system, either tightening (constricting) or relaxing (dilating).

Arterioles are the smallest arteries in the body. They deliver blood to capillaries. Arterioles are also capable of constricting or dilating and, by doing this, they control how much blood enters the capillaries.

Capillaries are tiny vessels that connect arterioles to venules. They have very thin walls which allow nutrients from the blood to pass into the body tissues. Waste products from body tissues can also pass into the capillaries. For this reason, capillaries are known as exchange vessels.

Groups of capillaries within a tissue reunite to form small veins called venules. Venules collect blood from capillaries and drain into veins.

Veins are the blood vessels that carry blood back to the heart. They may contain valves which stop blood flowing away from the heart.

How do the heart and blood vessels work?

The heart works by following a sequence of electrical signals that cause the muscles in the chambers of the heart to contract in a certain order. If these electrical signals change, the heart may not pump as well as it should.

The sequence of each heartbeat is as follows:

  • The sinoatrial node (SA node) in the right atrium is like a tiny in-built ‘timer’. It fires off an electrical impulse at regular intervals. (About 60-80 per minute when you are resting and faster when you exercise.) This controls your heart rate. Each impulse spreads across both atria, which causes them to contract. This pumps blood through one-way valves into the ventricles.
  • The electrical impulse gets to the atrioventricular node (AV node) at the lower right atrium. This acts like a ‘junction box’ and the impulse is delayed slightly. Most of the tissue between the atria and ventricles does not conduct the impulse. However, a thin band of conducting fibres called the atrioventricular bundle (AV bundle) acts like ‘wires’ and carries the impulse from the AV node to the ventricles.
  • The AV bundle splits into two – a right and a left branch. These then split into many tiny fibres (the Purkinje system) which carry the electrical impulse throughout the ventricles. The ventricles contract and pump blood through one-way valves into large arteries:
    • The arteries going from the right ventricle take blood to the lungs.
    • The arteries going from the left ventricle take blood to the rest of the body.
  • The heart then rests for a short time (diastole). Blood coming back to the heart from the large veins fills the atria during diastole:
    • The veins coming into the left atrium are from the lungs (full of oxygen).
    • The veins coming into the right atrium are from the rest of the body (depleted of oxygen).

The sequence then starts again for the next heartbeat. The closing of the valves in the heart make the ‘lub-dub’ sounds that a doctor can hear with a stethoscope.

If you exercise, your body tissues need more oxygen and will produce more carbon dioxide. This means your heart must speed up to meet those needs. How fast your heart beats (your heart rate) is controlled in a number of different ways. The brain controls the heart rate through the nervous system. A special part of the brain, called the medulla oblongata, receives information from many different systems of the body. The brain then co-ordinates the information and either sends signals to increase or decrease the heart rate, depending on what is necessary.

Even before physical activity begins, your heart may speed up in anticipation of what is to come. This is because a special part of the nervous system sends signals to the medulla. As physical activity starts, cells of the nervous system which monitor changes in the body (receptors) send signals about the position of your muscles to the brain. This can increase your heart rate.

The body also has other receptors which measure levels of chemicals, such as carbon dioxide, in your blood. If levels of carbon dioxide rise, signals are sent via the nervous system to the brain. The brain then sends electrical signals to the heart via nerves to speed it up. The signals cause the release of hormones which make the SA node fire more often. This means the heart beats more frequently. The brain can also send signals to the heart to slow it down.

Other hormones, such as those from the thyroid gland, can also influence your heart rate, as can certain substances found in your blood.

The most important function of the cardiovascular system (the heart and blood vessels together) is to keep blood flowing through capillaries. This allows capillary exchange to take place. Capillary exchange is the process of nutrients passing into the body’s cells and waste products passing out. Blood vessels are uniquely designed to allow this to happen.

Blood leaves the heart in the larger arteries. These vessels help to propel blood, even when the heart is not beating, because they have elastic walls which squeeze the blood in them. Arterioles are smaller than arteries and provide the link between the arteries and the capillaries. Capillaries allow nutrients and waste products to move in and out of the bloodstream. Venules take blood from the capillaries to the veins. Veins take blood back to the heart. This constant circulation of blood keeps us alive.

Your blood vessels also play a part in the regulation of your blood pressure. Certain chemicals in the body can cause our blood vessels either to tighten (contract) or to relax (dilate). Signals from our nervous system can also make our blood vessels relax or contract. These changes cause a change in the size of the lumen of the vessel. This is the space through which blood flows. In simple terms, constriction of blood vessels causes an increase in blood pressure. Dilation of blood vessels causes a decrease in blood pressure. However, blood vessels don’t just control blood pressure by themselves. Your body controls blood pressure using a complicated system. This involves hormones, signals from your brain and nervous system and the natural responses of your blood vessels. 

The blood supply to the heart

Like any other muscle, the heart muscle needs a good blood supply. The coronary arteries take blood to the heart muscle. These are the first arteries to branch off the large artery (aorta) which takes blood to the body from the left ventricle.

  • The right coronary artery mainly supplies the muscle of the right ventricle.
  • The left coronary artery quickly splits into two and supplies the rest of the heart muscle.
  • The main coronary arteries divide into many smaller branches to supply all the heart muscle.

Some disorders of the heart and blood vessels

File:Surface anatomy of the heart.svg

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Heart Anatomy Video | Medical Video Library

The heart is the most important muscular organ in the body. It works around the clock pumping blood to various parts of the body through the network of blood vessels. The normal adult heart weighs between 200- 425 grams (7 to 15 ounces) and is about the size of your fist. Learning about your heart and its functions can help you understand the various conditions that may affect your heart as well to take precautions to prevent them.

The heart is located between the right and left lungs in the middle of your chest. The heart’s function is to supply oxygen and blood to all parts of the body. Oxygenated blood pumped from the heart reaches the body’s organs through the systemic arteries, while veins carry impure or deoxygenated blood back to the heart.

The heart has four muscular chambers, the upper two chambers are called the right and left atria, and the lower two chambers are called the right and left ventricles.

For better understanding, the structures of the heart are discussed under two

Sections external anatomy and internal anatomy.

The external view of the heart shows many structures. Every structure is associated with certain function which is important for normal functioning of the heart. Let us learn more about these structures.

Pericardium: The pericardium is a fluid filled sac that encloses the heart and the ends of its major blood vessels including the aorta, vena cava and pulmonary artery. The pericardium is made of three layers:

1. Outer fibrous sac–fibrous pericardium,

2. Middle layer–parietal pericardium

3. Inner layer–visceral pericardium

The space between the parietal and visceral layer is called the pericardial cavity and is filled with pericardial fluid. The pericardial fluid acts as a lubricant to allow normal heart movements within the chest and also acts as a shock absorber to protect the heart from trauma

Arteries and Veins

Aorta: The aorta, the largest blood vessel in the body, carries oxygen rich blood from the left ventricle to the various parts of the body.

Vena Cava: The superior vena cava and inferior vena cava are the two largest veins in the body. The superior vena cava returns deoxygenated blood to the right atrium from the upper part of the body. The inferior vena cava brings deoxygenated blood from the lower part of the body to the right atrium of the heart.

Pulmonary artery and pulmonary veins: The pulmonary artery transports the de-oxygenated blood from the right ventricle to the lungs for oxygenation. The oxygenated blood is then carried to the left atrium through the pulmonary veins.

Coronary arteries and coronary veins: Coronary arteries originate from the ascending aorta and deliver oxygen-rich blood to the heart muscles. Coronary veins remove deoxygenated blood from the muscular tissue of the heart and drain it into the right atrium.

Internal Heart Anatomy

Muscular chambers: The heart has four muscular chambers, the upper two chambers are called the right and left atria, and the lower two chambers are called the right and left ventricles.

The right atrium collects the deoxygenated blood from the vena cava and delivers it to the right ventricle. This delivery is regulated by the tricuspid valve. The right ventricle delivers the blood to the lungs for purification (oxygenation). This delivery is regulated by the pulmonary valve.

The left atrium collects the oxygenated

blood from the lungs via the pulmonary veins and delivers it to the left ventricle. This delivery is regulated by the mitral valve. The left ventricle then delivers the oxygenated blood to the aorta (main artery) from where it is pumped to the rest of the body. This delivery is regulated by the aortic valve.

Heart Valves: Heart valves are flap-like structures that allow blood to flow in one direction preventing backward flow of the blood.

The heart has four valves :

Tricuspid Valve: It is located between the right atrium and the right ventricle.

Mitral Valve: It is located between the left atrium and the left ventricle.

Pulmonary Valve: It is located between the right ventricle and the pulmonary artery.

Aortic Valve: It is located between the left ventricle and the aorta.

Circulatory System of the Heart

The heart works as a pump to deliver blood to every organ, tissue, and cell of your body through a complex network of arteries, arterioles, and capillaries. Blood returns back to the heart through venules (small veins) and veins.

The circulatory system has two parts:

Pulmonary circulation: During pulmonary circulation, the pulmonary artery carries de-oxygenated blood from the heart to the lungs for oxygenation and returns oxygenated blood back to the heart through the pulmonary veins.

Systemic circulation: In systemic circulation, the aorta carries oxygenated blood from the heart to all the organs of the body through the systemic arteries, and returns de-oxygenated blood back to the heart via the systemic veins.

Conduction System.

The heart muscle consists of an electrical conduction system that triggers the heart walls to contract. The system is made of two nodes (special conduction cells) and a series of conduction pathways.

Sinoatrial or SA node: Also called the pacemaker of the heart, the SA node is located in the upper wall of the right atrium. The SA node is responsible for setting the rate and rhythm of the heart beat causing the atria to contract when the electrical impulse is released. The signal then passes to the atrioventricular (AV) node.

Atrioventricular (AV) node: Located between the atria and ventricles, the AV node checks the signal and sends it to the conduction pathways (bundle of His) to provide electrical stimulus to the ventricles.

Bundle of His: This is a group of fibers located within the septum of the heart that carries electrical impulses from the AV node to the ventricles. It is divided into right and left bundle branches. These bundle branches are further divided into tiny filaments, known as Purkinje fibers. These fibers connect directly to the cells in the walls of your heart’s left and right ventricles to maintain regular contraction.

A healthy heart is important for overall wellbeing. Certain disease conditions and lifestyle habits such as smoking, being overweight, and leading a sedentary life can put your heart at risk affecting how it

functions and leading to complications. Heart disease is preventable and the actions you take to reduce your risk of heart disease by making lifestyle changes will increase your chances for a long and healthy life.

 

Heart anatomy – MyDr.com.au

The heart is divided into 4 chambers: 2 on the right hand side and 2 on the left. Each upper chamber is known as an atrium and each lower chamber as a ventricle. The 4 compartments are known as: the right atrium; the right ventricle; the left atrium and the left ventricle. Blood comes into the heart via the atria, which are the smaller chambers, and is pumped out via the larger ones — the ventricles.

Right and left sides of the heart

The right hand side of the heart (shown on the left of pictures and diagrams) pumps blood needing oxygen to the lungs.

This blood goes to the lungs where it is loaded up with oxygen and sent back to the heart. The oxygen-rich blood enters the left side of the heart which then pumps it around the body to where it is needed.

Blood which has delivered its oxygen to the muscles and tissues then returns back to the right-hand side of the heart to start the cycle again.

Superior and inferior vena cavae

These are the 2 large veins which enter the heart on the right hand side and bring blood low in oxygen into the right atrium. The superior (top) vena cava brings in blood from the head and arms and upper body; the inferior (lower) vena cava brings in blood from the trunk and legs — the lower body.

Pulmonary arteries

The right and left pulmonary arteries branch off the main pulmonary trunk. Blood that needs oxygen is pumped into them from the right ventricle and they take it to the lungs where it is loaded up with oxygen.

Pulmonary veins

The right and left pulmonary veins bring the oxygen-rich blood back from the lungs to the heart into the left atrium.

Aorta

The aorta is the largest artery in the body. Blood full of oxygen is pumped by the left ventricle into the aorta, round the aortic arch and out into the upper body via the 3 main arteries branching off the aortic arch and into the thorax, trunk and lower body via the descending aorta.

Valves

Valves are one-way doors. There are valves separating the chambers of the heart. As the heart beats, the valves open and blood is pumped from one chamber to another chamber.

The right atrium and right ventricle are separated by the tricuspid valve. The tricuspid valve lets blood pump from the right atrium into the right ventricle but prevents its flow back again. Similarly, the mitral valve opens from the left atrium into the left ventricle.

The pulmonary valve and aortic valve are at the outlets of the right and left ventricles, respectively.

Heart valve disorders happen when the valves either allow blood to leak backwards, for example, mitral valve regurgitation, or the valves don’t open properly, as in mitral valve stenosis.

Coronary arteries

The heart is just a big muscle which pumps blood around the body. Like all your muscles, the heart needs oxygen to work. This oxygen is brought to the heart by the coronary arteries.

The right and left coronary arteries branch off the aorta — the large main blood vessel which leaves the heart with oxygen-rich blood — so they are ensured of a good blood supply rich in oxygen.

If the coronary arteries become narrowed by fatty deposits in the lining of the arteries (atherosclerosis) then the flow of blood to the heart muscle may be restricted. If the heart muscle doesn’t get enough blood it doesn’t get enough oxygen to work properly — this is called ischaemia.

Ischaemia can cause chest pain or discomfort (angina), often described as a feeling of pressure or tightness in the chest. Angina pain may also be felt in the neck, shoulders or arms. Angina is often brought on by physical activity, and typically improves with rest.

1. Tortora GJ, Derrickson BH. Essentials of Anatomy and Physiology. 9th International student edition. New York: Wiley; 2012.
2. Tracey DJ, Baume P. Anatomica: The Complete Reference to the Human Body and How it Works. Random House Australia, 2000.
3. Netter FH. Atlas of Human Anatomy. 6th ed. Saunders; 2014.

Queensland Cardiovascular Group | Anatomy of the Heart

The heart weighs between 200 and 425 grams and is a little larger than the size of your fist. It has a volume capacity of 80-100mls. By the end of a long life a person’s heart may have beat more than 3.5 billion times. In fact, each day the average heart beats about 100,000 times, pumping around 7500 litres of blood.

Your heart is located between your lungs in the middle of your chest, behind and slightly to the left of your breastbone. A double layered membrane called the pericardium surrounds your heart like a sac. The outer layer of the pericardium surrounds the roots of your hearts major blood vessels and is attached by ligaments to your spinal column, diaphragm and other parts of your body. The inner layer of the pericardium is attached to the heart muscle. A coating of fluid separates the two layers of membrane, letting the heart move as it beats, yet still be attached to your body.

Your heart has 4 chambers. The upper chambers are called the left and right atria and the lower chambers are called the left and right ventricles. A wall of muscle called the septum separates the left and right atria and the left and right ventricles. These are referred to as the atrial and ventricular septum. You may have heard your doctor refer to a condition called a ‘hole in the heart’. This simply means a tiny hole in the atrial septum separating the atria (called a PFO– Patent Foramen ovale or ASD—Atrial Septal Defect) or in the ventricular septum separating the ventricles (called a VSD—Ventricular Septal Defect). The left ventricle is the largest and strongest chamber in your heart.

The left ventricle’s chamber walls are only about 1.0 to 1.3cm, but they have enough force to push blood through the aortic valve and into your body.

Four types of valve regulate blood flow through your heart:

  1. The tricuspid valve regulates blood flow between the right atrium and right ventricle.
  2. The pulmonary valve controls blood flow from the right ventricle into the pulmonary arteries, which carry blood to your lungs to pick up oxygen.
  3. The mitral valve lets oxygen rich blood from your lungs pass from the left atrium into the left ventricle.
  4. The aortic valve opens the way for oxygen rich blood to pass from the left ventricle into the aorta, your body’s largest artery, where it is delivered to the rest of your body.

A more detailed description of blood flow through the heart is seen below.

Blood enters the right atrium of the heart through the superior vena cava. The right atrium contracts and pushes the blood cells through the tricuspid valve into the right ventricle. The right ventricle then contracts and pushes the blood through the pulmonary valve into the pulmonary artery, which takes it to the lungs. In the lungs, the blood cells exchange carbon dioxide for oxygen. The oxygenated blood returns to the heart via the pulmonary veins and enters the left atrium. The left atrium contracts and pumps the blood through the mitral valve into the left ventricle. Finally, the left ventricle contracts and pushes the blood into the aorta. The aorta branches off into several different arteries that pump the oxygenated blood to various parts of the body.

90,000 She had a heart – Everything interesting in art and not only. – LiveJournal

Anatomy of the Heart (She Had a Heart), Enrique Simone Lombardo

A little story of a big picture. She is generally outstanding, this picture. Very famous and revolutionary for that time. She makes a strong impression, excites a sense of reality. The canvas has two more names: “Anatomy of the Heart” and “Autopsy”.

Look — there is an anatomist, and his heart is in his hand…. And a sad, almost puzzled and incredulous expression on his face.
What confused the doctor?

Who is the girl on the breakout table?

Most are inclined to the point of view that she is a prostitute. The biographers of Simone himself tell about this.

Simone, when he left for Rome between 1888 and 1892, attended the autopsy in the morgue, where the body of a woman found in the Tiber fell.

Disenfranchised, without documents, they often ended their short life there.

Another argument is its appearance.
She has long red hair, which in painting has traditionally been associated with corrupt women from the Renaissance to the Pre-Raphaelite school.

She is somewhat reminiscent of the heroines of Toulouse-Lautrec in Parisian cabarets. The delicate skin tones of the heroine contrast with the gray lifeless walls, emphasizing the tragedy of the picture.

What is the doctor thinking?
Perhaps this is the first person in her life who thought that she had a heart.
The original title of the work “She Had a Heart” is just about that.

Old man Simone found on the street – for the role of an elderly doctor, he asked a colorful beggar to pose.
The painting was enthusiastically received by critics, brought the artist international recognition and several awards at exhibitions.

Here is another powerful piece of his: The Beheading of St. Paul. 1887
The picture is shocking – it is still poorly said.

Spectators often have a feeling of presence – as if a time machine had thrown onto the square where the execution takes place….

Enrique Simone i Lombardo (1866-1927) – an outstanding Spanish painter.
Enrique Simone i Lombardo was born on February 2, 1866 in Valencia.

Since childhood, he dreamed of becoming a priest, but the love of painting won, and Simone and Lombardo decided to link their lives with art.

First, the young man graduated from the Royal Academy of Arts of San Carlos in Valencia, then he moved to Malaga and entered the studio of the artist Bernardo Ferrandis Badenes, a native of Valencia.
Here Simone and Lombardo joined the community of artists of the city of Malaga.

War correspondent in Morocco in 1893-1894.
Winner of several international awards, including those received at exhibitions in Madrid (1892), Chicago (1893), Barcelona (1896) and Paris (1900).

Professor of the Royal Academy of Fine Arts of Sant Jordi in Barcelona since 1901.

Since 1911, member of the Royal Academy of Fine Arts of San Fernando in Madrid.

“She Had a Heart” | More than once enchanted wanderer

Hello everyone!

There are pictures that are difficult to pass by. They catch on, make you think and empathize. Of course, all artists dream that it is their painting that will evoke a deep emotional response. But not everyone succeeds.

In this post I have selected a few pictures that do not leave me indifferent.They are united by a common detail. Their heroines HAD a heart.

The post was inspired by a plot from “Arc de Triomphe”, where the main character lost his patient, because she did not dare to ask for help in time. Whoever has read it will probably remember, whoever has not read it – I recommend it.

“And I had a heart.” Enrique Simone Lombardo. 1890

“And I had a heart.” Enrique Simone Lombardo. 1890

“And I Had a Heart” is definitely a masterful painting, both in terms of technique and in terms of emotional charge.In a bare gray room that looks like a morgue, the body of a young girl lies on a table. We do not know what happened to her, but whatever her fate was, the heroine certainly did not dream of such an ending. Life left her, erasing the shades of pink, giving the skin a marble hue.

Above the corpse is an elderly doctor who, according to all the canons of justice, should not have survived the girl. But who said that life is subject to such canons? The doctor carefully examines the heart, which until recently was beating in the chest, loved someone, worried about someone.He is the only one alive in this abode of death. And the mistress of the heart is no longer the mistress, but just another source of samples for science …

“Path”. Romain Brooks. 1911

“Path”. Romain Brooks. 1911

Even more laconic is the painting by the American artist she called “The path”. The word can be translated as “path” or “path”, but the poetic (and in my opinion) more precise context is “path”.

The body of a dead woman lies in the moonlight, and it seems that the light itself and the woman’s hair are flowing, dissolving and melting in darkness, plunging into hopeless nothingness.The final point of the path. What brought her to her so early? No answer …

Death of Cleopatra. Jean-Andre Rixant. 1884

“The Death of Cleopatra”. Jean-Andre Rixant. 1884

Thanks to the trend in art at that time – Orientalism – the plot looks more or less believable. At least in the interiors and clothes Egypt is guessed. Previously, Cleopatra in most cases was portrayed wearing modern artist costumes.

The plot here is half historical, half mythical.Having lost her beloved and not wanting to return to Rome as a precious trophy, the ruler of Egypt chose death. Legend has it that a maid brought her a snake in a basket of figs. And the queen forced the snake to bite her. Therefore, there is often a snake in paintings on this topic.

They say that along with the body of Cleopatra, the bodies of two of her faithful maids were also found. And the snake was not found in the room. It is unlikely that the snake stung all three to death, evenly distributing the poison. Most likely they were poisoned.Moreover, not long before that Cleopatra personally supervised the experiments, where she gave poisons to those sentenced to death and watched their action, figuring out which of the poisons bestows the easiest death …

“Ophelia”. John Everett Millais. 1851

Ophelia. John Everett Millais. 1851

The only completely fictional plot in which death has not yet occurred, strictly speaking. This is Ophelia, a character in the Shakespearean drama Hamlet.

Art critics are still arguing whether Ophelia died in an accident or drowned.Shakespeare himself does not give an exact answer with his text. According to the plot, Ophelia was first damaged by her mind. And then the following happened:

There is a willow tree above the stream, which bends
Gray leaves to the mirror of the wave;
There she came, weaving into garlands
Nettles, buttercup, iris, orchids, –
Free shepherds have a coarser name,
For humble virgins, they are the fingers of the dead:
She tried to hang on the branches
Her wreaths; the insidious bough broke,
And the herbs and she herself fell
Into the weeping stream.Her clothes,
Stretched out, carried her like a nymph;
She, meanwhile, sang fragments of songs,
As if she had not sensed trouble
Or was a creature born
In the element of waters; it could not last,
And the clothes, heavily drunk,
The unhappy from the sounds was carried away
Into the swamp of death.

It is believed that Shakespeare did not invent this plot, but only embellished it. When he was sixteen in his hometown of Stratford, a girl drowned in the Avon River. Officially, she slipped on the bridge, but it was rumored that she could and will rush because of unrequited love.Who knows, maybe her reckless sacrifice served as the prototype for the well-known heroine, indirectly perpetuating the memory of the unfortunate one? ..

“The Drowned Man”. Perov. 1867

“The Drowned Woman”. Perov. 1867

Well, Perov’s fantastic canvas completes my selection, returning it to the circles of realism. A gloomy city covered with fog and smog, the mud of the old pier and the indifferent policeman, who has already seen such drowned women. Against the background of such scenery, the death of the girl is seen as a kind of liberation.Her face is serene and calm. All the fuss and sadness is already behind …

Here’s a selection. The author’s work can be marked with a like, and do not forget to subscribe to the channel so as not to miss my new post.

Patient of St. Luke – “InfoMedPharmDialogue”

The painting got into the palazzo only in 2011, the Italian state bought it from a private collection. According to experts, the painting by Giovanni Lanfranco, one of the masters of the Italian Baroque, was completed around 1620.The painting depicts an elderly man holding a small child by the wrist, and a young woman (most likely the child’s mother) stands behind them, her gaze turned to the elder, probably a healer. The mother looks at the elderly man with hope. With her right hand she supports the child, and with her left hand she points to the poor child – she came for help. The elder holds the child’s limp hand, looks up, as if asking Heaven for help in healing.

A thin rim of glow, or a nimbus, is seen over the head of the elder – an iconographic symbol of divinity.Religious painting standards make it possible to identify the elder as Saint Luke, the apostle, the revered author of one of the four Gospels. Luke was a physician (Col. 4:14), possibly a ship’s doctor. The Muratorian Canon reports that Luke was also an expert in law, in addition, in the Orthodox and Catholic traditions, he is considered the first painter, since it was he who created the first portrait of the Virgin Mary. There is a book at his knees, on the spine of which is read the inscription: “Hippocrates.”

This depiction of Luca, both a doctor and an artist, is considered unprecedented in Italian art.But even more interesting is the image of the child whom Luke must heal. This baby is the emotional center of the picture.

The child looks sick not only because his hand is limply hanging in St. Luke’s hand, and his mother is holding his back, as if afraid that he is about to fall. Judging by the proportions, the baby is about 3 years old or slightly older. His skin color is very different from his mother: gray, with an earthy tint. To create this “unhealthy” color, the artist used bluish colors.The child’s sclera are ashy gray. It seems that the boy cannot stand on his own, even his head bows to his mother’s hand – perhaps he is too weak to hold his own head. Unlike the gaze of a man and a woman, the gaze of a child is not fixed, but is directed to no one knows where. The baby’s abdomen is greatly enlarged, and his eyes and face are swollen. The child has ascites.

The word “ascites”, denoting abnormal accumulation of fluid in the abdominal cavity, is of Greek origin (askites / askhos) and means “bag”, “bladder” or “storage container”.Ascites can occur at any age and even in utero.

The painting is called “St. Luke Healing a Swollen Child” (S. Luca guarisce il bambino idropico). The word “idropico” in Italian clearly indicates “dropsy” (“idropico” has a common origin with the Greek “hydrops”). Previously, this term was used to describe any excess fluid accumulation, including edema, then it was replaced by the term “abdominal dropsy” or ascites to refer to fluid in the abdomen.

Anatomy of the Heart Season 2: When It Comes Out (TV Series)

There is nothing superfluous in the human body. Each organ, vessel, bone is a small or large part of the overall system. But people have the most reverent attitude to their hearts, because it is believed that thanks to this organ one can feel, do good or evil, love … and life path. However, their fates are intertwined, bringing in more and more events and experiences …

Genre – melodrama.
The premiere of the 1st season took place on May 24, 2021 on Channel One (12 episodes).

When is Anatomy of the Heart Season 2 coming out?

Anatomy of the Heart showed the story of several couples who had to go through a difficult life path. Director Maxim Kubrinsky revealed all the themes in the series, so the continuation of the picture is not planned . At the moment, Kubrinsky is working on other projects.

Plot

Late 80s – early 90s.The USSR is going through difficult times, but people continue to live, make plans, dream and love. The tenth grader Marina Korshunova really fell in love. The girl does not see life without Boris, but her parents are categorically against this union. Despite her father’s threats, Marina invites Boris to her home. After 9 months, a girl is born with a heart defect. To avoid difficulties, Nikolai Korshunov assigns the baby to an orphanage, and informs his daughter about her death.

Still from the series

Once upon a time, Doctor Dmitry Voskresensky received an offer from his Italian colleagues to stay in their country.Wouldn’t that be a betrayal by the cardiologist? Years passed, Voskresensky performed in Moscow a brilliant operation according to his own method, eliminating a congenital heart defect of a girl from an orphanage. After the girl was on the mend, Voskresensky took Zoya to his home. The orphan is the same girl, the daughter of Marina and Boris …

Main characters

  • Nikolai Korshunov – director of a large chemical plant; brings up her only daughter and takes care of her too – Konstantin Milovanov.
  • Zinaida – Nikolai’s wife; against the daughter’s relationship with Boris, turns her husband against the guy; jealous of her husband for Boris’s mother – Anna Dubrovskaya.
  • Marina – daughter of Nikolai and Zina; 10-grader, in love with Boris, the father is categorically against this connection; but the unexpected happens – Marina becomes pregnant, then a girl with a severe heart defect is born, the life of the newborn is in danger – Ksenia Plyusnina.
  • Yuri Belsky – cardiologist, received an offer to stay to work in Italy with Dmitry Voskresensky – Andrei Rudensky.
  • Natalya – Yuri’s wife; gets into a difficult life situation due to the betrayal of her husband and difficulties in the personal life of Boris – Daniela Stoyanovich.
  • Boris – son of Yuri and Natalia; preparing to enter the institute; in love with Marina and is ready to marry her – Ilya Korobko.
  • Dmitry Voskresensky – cardiologist, married, but no children; Ministry of Health is eyeing a promising gifted doctor; took up a girl from an orphanage, who underwent a successful heart operation – Kirill Grebenshchikov.
  • Olga – Dmitry’s wife; dreamed of conquering the world of ballet, but could not reach the desired heights –
    Olga Lomonosova.
  • Zoya – a girl born with a heart defect; was transferred to an orphanage; Voskresensky takes over the operation, and Dina Bukhman operates it in Moscow.

Interesting facts

  1. The series was directed by Maxim Kubrinsky, who worked on such projects as “Shaman”, “Sea Devils”, etc.Kubrinsky was personally looking for an actress for the role of Marina, because she had to have a certain Soviet appearance. Having found the portfolio of Ksenia Plyusnina, the director sent her an invitation to audition. For the theatrical actress, the role in the series became her debut.
  2. The working title of the series is “Tetrad of Fallot”. It is a medical term for a type of congenital heart disease. It is believed that Tetralogy of Fallot is more common in boys, with a similar diagnosis accounting for 1 infant in every 1000 newborns with a heart defect.
  3. The main locations for filming were selected in 3 cities: Moscow, Yaroslavl and Feodosia (Crimea). The filming process lasted 9 months.
  4. Few people know, but the brilliant surgeon Dmitry Voskresensky, played by the actor Kirill Grebenshchikov, has a real prototype. This is Vitaly Alekseevich Bukharin, a Soviet surgeon who developed an original method of surgical intervention. Having defended his doctoral dissertation on the topic “Tetrad of Fallot”, Vitaly Alekseevich began to actively apply his own methodology in practice, saving the lives of children.
  5. Kirill Grebenshchikov carefully prepared for his role. To do this, he consulted with current cardiac surgeons, and also got acquainted with archival documents. We add that Kirill had already played a doctor when he got the role of neonatologist Andrei Lazarev in the series “Pregnancy Test”. Neonatologists work with neonatal pathologies.

Anatomy of the Heart Season 2: Episode

  • 902×05 Series

    unannounced 2×05

    unannounced 2×05 Series

    Series 6

  • not announced

    Episode Episode Name Released
    2×01 Episode 1 not announced

  • 21 Episode 902 2
  • unannounced
    2×03 Series 3 unannounced
    2×04 Series 4 unannounced
    unannounced
    2×07 Series 7 unannounced
    2×08 Series 8 unannounced
    2×09 Series

  • Series 10 not announced 902 21

    5 Best Love Series

    Myocardial Infarction

    Myocardial infarction is one of the clinical forms of ischemic heart disease, occurring with the development of ischemic necrosis of the myocardial area, caused by absolute or relative insufficiency of its blood supply.

    On December 1, 2012, the American College of Cardiology and the American Heart Association published the most recent clinical guidelines for the management of persistent ST-segment elevation ECG myocardial infarction and its early complications [1] . Earlier in October 2012, the European Society of Cardiology [2] updated its recommendations for this form of the disease. The latest updates to their recommendations for the management of acute coronary syndrome without persistent ST-segment elevations on ECG were published in May [3] and December [4] 2011, respectively.

    Classification

    By developmental stages:

    1. Acute period (up to 2 hours from the onset of myocardial infarction)
    2. Acute period (up to 10 days from the onset of myocardial infarction)
    3. Subacute period (from 10 days to 4-8 weeks)
    4. Scarring period (from 4-8 weeks to 6 months)

    According to the lesion anatomy:

    1. Transmural
    2. Intramural
    3. Subendocardial
    4. Subepicardial

    By the volume of the lesion

    1. Croupous-mucous
    2. Small focal, non-Q-infarction
    • Localization of the necrosis focus.
      1. Left ventricular myocardial infarction (anterior, lateral, inferior, posterior).
      2. Isolated apex myocardial infarction.
      3. Interventricular septal myocardial infarction (septal).
      4. Right ventricular myocardial infarction.
      5. Combined localizations: posterior-inferior, anterior-lateral, etc.

    Downstream:

    1. Monocyclic
    2. Protracted
    3. Recurrent myocardial infarction (in the 1st coronary artery falls asleep from a new focus to 72 hours )
    4. Repeated MI (in dr.cor. art., new necrosis after 28 days from previous MI)

    Clinical classification prepared by a joint working group of the European Society of Cardiology, American College of Heart, American Heart Association and World Heart Federation (2007) [5] :

    • Spontaneous MI (type 1) associated with ischemia due to a primary coronary event such as plaque erosion and / or destruction, cracking, or dissection.
    • Secondary myocardial infarction (type 2) associated with ischemia caused by an increase in oxygen deficiency or oxygen supply, for example, with coronary spasm, coronary embolism, anemia, arrhythmia, hyper- or hypotension.
    • Sudden coronary death (type 3), including cardiac arrest, often with symptoms of suspected myocardial ischemia with expected new ST elevation and new left bundle branch block, detection of fresh coronary artery thrombus on angiography and / or autopsy, and death before specimen collection blood or before an increase in the concentration of markers.
    • PCI-associated MI (type 4a).
    • MI associated with stent thrombosis (type 4b), confirmed by angiography or autopsy.
    • CABG-associated MI (type 5).

    It should be borne in mind that sometimes patients may experience several types of MI simultaneously or sequentially. It should be noted that the term “myocardial infarction” is not included in the concept of “necrosis of cardiomyocytes” due to CABG (opening in the ventricle, manipulation of the heart) and the influence of the following factors: renal and heart failure, cardiac stimulation, electrophysiological ablation, sepsis, myocarditis, action of cardiotropic poisons, infiltrative diseases.

    Etiology

    Myocardial infarction develops as a result of obstruction of the lumen of the vessel supplying the myocardium (coronary artery). The reasons may be (according to the frequency of occurrence):

    1. Atherosclerosis of the coronary arteries (thrombosis, obstruction by plaque) 93-98%
    2. Surgical obturation (ligation of the artery or dissection during angioplasty)
    3. Embolization of the coronary artery (thrombosis, with
    4. Spasm of the coronary arteries

    Separately, infarction is isolated in case of heart defects (abnormal discharge of the coronary arteries from the aorta).

    Risk factors

    Main article: Risk factors for coronary heart disease
    Main article: Cardiovascular risk

    • Tobacco smoking and secondhand smoke [6]
    • Arterial hypertension
    • Rheumatic carditis
    • concentration of LDL (“bad”) cholesterol in the blood

    • Low concentration of HDL (“good”) cholesterol in the blood
    • High blood triglycerides
    • Low level of physical activity
    • Age
    • Air pollution [7]
    • Sex (Men more often suffer from myocardial infarction than women)
    • Obesity [8]
    • Alcoholism
    • Diabetes mellitus
    • Myocardial infarction in the past and manifestation of any other manifestations of atherosclerosis

    Differ adia:

    1. Ischemia
    2. Damage (necrobiosis)
    3. Necrosis
    4. Scarring

    Ischemia can be a precursor of a heart attack and last for quite a long time.At the heart of the process is a violation of myocardial hemodynamics. Usually, narrowing of the lumen of the artery of the heart is considered clinically significant to such an extent that the restriction of blood supply to the myocardium can no longer be compensated. Most often this occurs when the artery is narrowed by 70% of its cross-sectional area. When compensatory mechanisms are exhausted, they talk about damage, then metabolism and myocardial function suffer. Changes can be reversible (ischemia). The damage stage lasts from 4 to 7 hours. Necrosis is characterized by the irreversibility of damage.1-2 weeks after a heart attack, the necrotic area begins to be replaced by scar tissue. The final scar formation occurs in 1-2 months.

    Clinical picture

    The main clinical sign is intense chest pain (anginal pain). However, pain can be variable in nature. The patient may complain of discomfort in the chest, pain in the abdomen, throat, arm, shoulder blade [9] . Often, the disease is painless in nature, which is typical for patients with diabetes mellitus.

    Pain syndrome persists for more than 15 minutes (can last 1 hour) and stops after a few hours, or after the use of narcotic analgesics, nitrates are ineffective. There is profuse (sticky) sweat [unknown term] .

    In 20-40% of cases with large-focal lesions, signs of heart failure develop. Patients report shortness of breath, unproductive cough.

    Arrhythmias are common. As a rule, these are various forms of extrasystoles or atrial fibrillation.Sudden cardiac arrest is often the only symptom of myocardial infarction.

    The predisposing factor is physical activity, psychoemotional stress, fatigue, hypertensive crisis.

    Atypical forms of myocardial infarction

    In some cases, the symptoms of myocardial infarction may be atypical. This clinical picture makes it difficult to diagnose myocardial infarction. There are the following atypical forms of myocardial infarction:

    • Abdominal form – symptoms of a heart attack are represented by pain in the upper abdomen, hiccups, bloating, nausea, vomiting.In this case, the symptoms of a heart attack may resemble those of acute pancreatitis.
    • Asthmatic form – symptoms of a heart attack are represented by increasing shortness of breath. The symptoms of a heart attack resemble those of an attack of bronchial asthma.
    • Painless myocardial ischemia is rare. Weakness is possible. Such a development of a heart attack is most typical for patients with diabetes mellitus, in whom sensory impairment is one of the manifestations of the disease (diabetes).
    • Cerebral form – symptoms of a heart attack are represented by dizziness, impaired consciousness, neurological symptoms; violation of understanding going on around.
    • Collaptoid form – begins with the development of collapse; the clinic is dominated by a sharp sudden arterial hypotension, dizziness, the appearance of cold sweat, darkening in the eyes. It is regarded as a manifestation of cardiogenic shock.
    • Arrhythmic form – begins with a paroxysm of cardiac arrhythmias;
    • Peripheral – differs in the localization of pain not in the retrosternal or precordial region, but in the throat, in the left hand, the end of the left little finger, in the cervicothoracic spine, and the lower jaw.
    • Edematous – the patient develops shortness of breath, weakness, swelling and even ascites relatively quickly, the liver enlarges – that is, acute right ventricular failure develops.
    • Combined – combines various manifestations of several atypical forms.

    Diagnosis

    Pain areas in myocardial infarction: dark red = typical area, light red = other possible areas.

    Back view.

    1. Early:
      1. Electrocardiography
      2. Echocardiography
      3. Blood test for cardiotropic proteins (MB-CPK, AST, LDH 1 , troponin [10] )
    2. Coronary artery disease (currently rarely used)
  • ECG descriptions for myocardial infarction

    Stage of developing myocardial infarction (0-6 hours)

    Stage of developing myocardial infarction

    • Dome-shaped ST segment above the isoline of ST
    • Segment segment
    • R wave high
    • Q wave low

    Acute stage of myocardial infarction (6-7 days)

    Acute stage of myocardial infarction

    • Negative T wave
    • Decrease in the amplitude of the R wave
    • Deepening of the R wave
    • Deepening myocardium (7-28 days)

      Healing infarction m Iocardium

      • Negative T wave
      • ST segment approaching the isoline

      Healed myocardial infarction (on the 29th day – up to several years)

      Healed myocardial infarction

      • Persistent Q wave
      • Decreased T156 amplitude

      • Decreased R156
      • ST complex on the isoline [11]

      Complications

      Early:

      Late:

      Treatment

      First aid

      • If a myocardial infarction is suspected, the patient is first seated and reassured.A sitting position is recommended, preferably on a chair with a backrest, or reclining with bent knees. Unbuttoned tight interfering clothing, loosen tie [15] .
      • If the patient is prescribed a medicine for chest pain, such as nitroglycerin, and the medicine is on hand, the patient is given that medicine [16] .
      • If the pain persists within 3 minutes after sitting alone or after taking nitroglycerin, an ambulance is called without delay. First aid providers should not succumb to the patient’s persuasion that everything will now pass [16] .If the ambulance cannot arrive quickly, the patient is taken to the hospital in a passing car. At the same time, it is advisable to have two healthy people in the car, so that one drives the car, and the other monitors the patient’s condition [17] .
      • If aspirin is at hand, and the patient does not have an allergy known to aspirin, then he is given 300 mg of aspirin to chew. If the patient is constantly taking aspirin, the dose taken that day is supplemented to 300 mg. It is important to chew the tablets or the aspirin will not work quickly enough [15] [17] .
      • In case of cardiac arrest (loss of consciousness, absent or agonal breathing), immediately begin CPR. Its use greatly increases the patient’s chances of survival. The use of portable defibrillators increases the survival rate even more: being in a public place (cafe, airport, etc.), first aid providers need to inquire with the staff about the presence of a defibrillator or a defibrillator nearby. Determination of the absence of a pulse is no longer a prerequisite for the initiation of resuscitation; loss of consciousness and lack of rhythmic breathing are sufficient [18] .

      Medical care

      Early treatment, if possible, is reduced to the elimination of pain, restoration of coronary blood flow (thrombolytic therapy, angioplasty of the coronary arteries, CABG). With severe heart failure in a clinic, it is possible to set intra-aortic balloon counterpulsation.

      Elimination of pain, shortness of breath and anxiety [edit | edit wiki text]

      If pain persists when the ambulance team arrives, the doctor uses morphine.Previously, 10 mg of morphine hydrochloride is diluted in 10 ml of 0.9% sodium chloride solution or distilled water. The first dose of 2-5 mg (that is, 2-5 ml of solution) is injected intravenously. Then 2-5 mg are additionally administered every 5-15 minutes until pain or side effects are eliminated.

      Administration of morphine in myocardial infarction without ST-segment elevation increases the risk of death [19] .

      It is also possible to use neuroleptanalgesia for anesthetic purposes – a combination of the narcotic analgesic fentanyl (0.05-0.1 mg) and the neuroleptic droperidol (2.5-10 mg, depending on the level of blood pressure).If necessary, neuroleptanalgesia is repeated at a lower dose.

      If the patient has arterial hypoxemia (arterial oxygen saturation <90%), shortness of breath or other signs of heart failure, humidified oxygen is given (through a mask or nasal catheter) at a rate of 2-5 l / min. Arterial hypoxemia, if possible, is determined using pulse oximetry.

      Despite this, systematic reviews in 2009 and 2010 showed that the use of oxygen in myocardial infarction increases the risk of death and the zone of necrosis, therefore at the moment it is not recommended to use oxygen therapy routinely [20] [21] .

      A patient with severe agitation, anxiety, fear (which does not disappear after the administration of a narcotic analgesic) can be prescribed a tranquilizer (for example, diazepam intravenously 2.5-10 mg). It is also important to reassure the patient and those close to him.

      Antiplatelet therapy

      All people with signs of acute coronary syndrome (myocardial infarction or primary unstable angina pectoris) who are not taking this medication and without contraindications to it should take acetylsalicylic acid, first chewed, in the first loading dose of 162-325 mg 903 1] [3] [22] [23] (or 150-300 mg according to European guidelines [2] [4] ).For these purposes, the enteric-soluble form is not suitable, since the onset of its action is slow. With severe nausea, vomiting, concomitant diseases of the stomach, intravenous administration of acetylsalicylic acid at a dose of 250-500 mg is possible. Further, acetylsalicylic acid is shown to such patients for life at a dose of 75-162 mg / day [24] . If there are contraindications to acetylsalicylic acid, clopidogrel is used in the first loading dose of 300 mg and then 75 mg / day [25] [26] .The combination of clopidogrel with aspirin is more effective than aspirin monotherapy for myocardial infarction without ST-segment elevation (without a statistically significant effect on mortality) and is economically justified when costs of the order of £ 6,078 for each additional year of full life (quality-adjusted life year ( QALY)) [27] . Routine addition of clopidogrel to aspirin for the conservative treatment of acute coronary syndrome without ST-segment elevation, as well as the placement of a metal stent without the application of a cytostatic and a stent coated with a cytostatic was recommended by the American College of Cardiology in 2007 [22] .In 2011, these recommendations were slightly adjusted – in particular, as an analogue of clopidogrel (75 mg / day) when installing stents, prasugrel was recommended at 10 mg per day [3] .

      Anticoagulants

      Use unfractionated heparin for 48 hours.At the beginning, 60 IU / kg (but not more than 4000 IU) is injected intravenously, then continuously intravenously at an initial rate of 13 IU / kg / h (but not more than 100 IU / h ) The further dose is selected, focusing on the APTT, which should be 1.5-2 times more than the norm and be monitored after 3, 6, 12, 24 hours.

      It is also possible to use low molecular weight heparin (enoxaparin), which is injected under the skin of the abdomen at a dose of 1 mg / kg 2 times a day for up to 5-7 days. 15 minutes before the first subcutaneous injection, 30 mg of this drug must be injected intravenously. The dose of the first 2 subcutaneous injections is no more than 100 mg. The advantages of low molecular weight heparin over unfractionated heparin: ease of administration and there is no need for constant monitoring of blood coagulation.

      Sometimes fondaparinux is used at a dose of 2.5 mg under the skin of the abdomen once a day.This drug is the most convenient to use and, unlike heparin, causes thrombocytopenia in more rare cases.

      Thrombolytic therapy

      Thrombolytic therapy is indicated for myocardial infarction with ST-segment elevation on the ECG. Its effectiveness has been convincingly proven, it allows to restore coronary blood flow, limit the size of myocardial infarction and reduce mortality. Thrombolysis is performed as early as possible and within 12 hours from the onset of the disease. For this, streptokinase is used at a dose of 1.5 million IU intravenously per 100 ml of 0.9% sodium chloride solution for 30-60 minutes.Alteplase is also used per 100-200 ml of isotonic solution according to the scheme: 15 mg intravenously in a stream, then 0.75 mg / kg for 30 minutes (but not more than 50 mg) and then 0.5 mg / kg for 60 minutes (but not more than 35 mg). Alteplase has advantages over streptokinase in the form of a more efficient restoration of coronary blood flow due to the thrombus tropism for fibrin, as well as the absence of antigenicity.

      Beta-blockers

      In the absence of contraindications, metoprolol, propranolol or atenolol are used.However, the effectiveness of intravenous use of beta-blockers in the early stages has not been proven and increases the risk of developing cardiogenic shock. Although some reports suggest treating a patient with a heart attack during transport to hospital with metoprolol can significantly reduce heart damage in myocardial infarction [28]

      Treatment of myocardial infarction with stem cells and exosomes

      Currently, therapy for myocardial infarction with stem cells actively researched in experiments on animals; There have been no clinical trials in humans to prove the effectiveness of this technique.Despite the fact that in experiments on animals stem cells have a positive effect, the issue of their treatment is clearly insufficiently studied for the transition to experiments on humans.

      In an experiment on rats, it was shown that the mobilization of stem cells under the influence of colony-stimulating factors accelerates the myocardial repair processes after a heart attack, with almost no scar remains [29] .

      A systematic review published by the Cochrane Collaboration in 2012 reported that stem cell therapy can significantly improve prognosis in acute myocardial infarction [30] .

      In animal experiments, even a single injection of exosomes of mesenchymal stem cells reduces the size of the infarction and improves the condition of the experimental. Obviously, exosomes compensate for the deficiency of enzymes that are important for supplying the cell with energy, and hence for the speedy rehabilitation of the heart muscle [31] [32] .

      Mental changes and psychoses

      With myocardial infarction, mental changes of a neurotic and neurosis-like nature are possible.These changes are based on the reaction of the individual to a serious, life-threatening illness. In addition to personality traits, the mental state of a patient with MI is also determined by somatogenic and external (environmental) factors (psychological influence of medical personnel, relatives, other patients, etc.).

      A distinction should be made between adequate (normal) and pathological (neurotic) reactions. The response to the disease is qualified as adequate if: a) the patient’s behavior, his feelings and ideas about the disease correspond to the information received from the doctor about the severity of myocardial infarction and its possible consequences; b) the patient adheres to the regimen, follows the doctor’s instructions; and c) the patient is able to control his emotions.

      Among the pathological reactions in more than 40% of cases, there is a cardiophobic reaction, in which patients experience fear of repeated MI and sudden death from a heart attack. Such patients are overly cautious, especially when trying to expand the regime of physical activity. An increase in fear is accompanied by tremors in the body, weakness, sweating, palpitations, and a feeling of lack of air.

      Depressive (anxious-depressive) reaction is also possible as one of the pathological reactions in MI.A depressed mood is noted. Patients do not believe in the possibility of a favorable course of the disease, experience internal tension, a presentiment of impending disaster, fear for the outcome of the disease, anxiety for the well-being of the family. Sleep disturbances, motor restlessness, sweating, and heart palpitations are characteristic.

      Much less often, mainly in the elderly, there is a hypochondriacal (depressive-hypochondriacal) reaction. With her, there is a constant and explicit overestimation of the severity of his condition, the inconsistency of the abundance of complaints with objective somatic changes, excessive fixation of attention on the state of his health.

      Anosognosic reaction is fraught with complications, in which there is a denial of the disease with disregard of medical recommendations and gross violations of the regime.

      In some cases, there is a hysterical reaction. The patient’s behavior is characterized by egocentrism, demonstrativeness, the desire to attract the attention of others, to arouse sympathy, emotional lability.

      The above mental changes are observed against the background of mental asthenia: general weakness, rapid fatigue with slight physical or mental stress, vulnerability, increased excitability, sleep disturbances, and vascular instability.

      Mental asthenia is more pronounced with prolonged bed rest and in elderly patients.

      If you do not carry out special measures, the changes in the psyche are aggravated, become persistent and in the future can significantly impede rehabilitation up to mental disability.

      One of the most formidable complications of the acute period of the disease – psychoses, which are observed in about 6-7% of cases. Gross behavioral disturbances, abrupt autonomic shifts are accompanied by a significant deterioration in the somatic state, with psychosis more often death occurs.In the vast majority of cases, psychoses develop in the 1st week of the disease. Their duration usually does not exceed 2-5 days.

      The main causes of psychoses in myocardial infarction are intoxication with decay products from a necrotic focus in the myocardium, deterioration of cerebral hemodynamics and hypoxemia caused by impaired cardiac activity. It is no coincidence that psychoses are most often observed in patients with extensive myocardial lesions and acute circulatory failure (cardiogenic shock, pulmonary edema).

      Brain lesions of various nature (consequences of traumatic brain injury, chronic alcoholism, cerebral atherosclerosis, hypertension, etc.) and old age predispose to the onset of psychosis in MI.

      Most often, psychosis occurs in the evening and at night. As a rule, it proceeds in the form of delirium. Consciousness is impaired with a loss of orientation in the environment and in time, illusions and hallucinations (more often visual) appear, the patient experiences anxiety and fear, motor restlessness increases, leading to motor excitement (incessant attempts to get out of bed, run out into the corridor, climb out the window and T.etc.). Often, delirium is preceded by a state of euphoria – an elevated mood with a denial of the disease and a gross overestimation of one’s strengths and capabilities.

      In elderly patients, the so-called subsonic states are sometimes observed: the patient, waking up at night, gets up, despite the strict bed rest, and begins to wander along the hospital corridor, not realizing that he is seriously ill and is in the hospital.

      Prophylaxis

      • Antithrombotic therapy with aspirin and / or clopidogrel reduces the risk of recurrent myocardial infarction.The use of clopidogrel and aspirin reduces the risk of cardiovascular events, but at the same time increases the risk of bleeding [33] .
      • Beta-blockers can be used to prevent myocardial infarction in people with a history of myocardial infarction [34] . Of all the beta-blockers, bisoprolol, metoprolol, succinate and carvedilol improve the prognosis in people with a reduced left ventricular ejection fraction below 40% [35] . Beta-blockers after myocardial infarction reduce mortality and morbidity.
      • Statin therapy after myocardial infarction reduces mortality [36] [37] .
      • The use of long-chain polyunsaturated omega-3 fatty acids (docosahexaenoic and eicosapentaenoic) in high doses also improves the prognosis after myocardial infarction [38] [39] [40] .
      • The use of intravenous unfractionated heparin or subcutaneous low molecular weight heparin in persons with primary unstable angina reduces the risk of myocardial infarction [41] .
      • ACE inhibitors are also used to prevent myocardial infarction in people with reduced left ventricular ejection fraction below 40% [42] .

      Prognosis

      The prognosis of the disease is conditionally unfavorable, after the onset of a heart attack, irreversible ischemic changes develop in the myocardium, which can lead to complications of varying severity.

      From Wikipedia – the free encyclopedia

      90,000 Congenital heart defects: pathological anatomy, clinical presentation, treatment and general clinical signs abstract on medicine

      Congenital heart defects: pathological anatomy, clinical picture, treatment and general clinical signs Transposition of great vessels – aortic discharge from the right ventricle and pulmonary artery from the left …The transposition of vessels without defects in the septa of the heart is incompatible with life; defects in the septa while heart defects somewhat compensate for severe circulatory disorders. For example, with transposition of vessels in combination with a defect of the interventricular septum, arterial blood passes from the left to the right ventricle, mixes here and passes into the aorta, and venous blood passes from the right into the left ventricle and then into the pulmonary artery. The larger the defect in the interventricular (or interatrial) septum, the better the oxygen supply to the body.The vast majority of patients with this heart defect die during infancy. A true common arterial trunk with a two-chambered heart is characterized by a common atrium and a common ventricle, from which the common arterial trunk departs, which arose in embryogenesis from the VI left aortic arch. The ascending aorta is not developed and is a connective tissue cord. Venous and arterial blood mixes in the common atrium. Arterio-venous blood enters the common ventricle, and then into the common arterial trunk, into the right and left branches of the pulmonary artery and into the systemic circulation through the botalle duct.With a common arterial trunk with a two-chambered heart, patients die a few days after birth. With a true common arterial trunk with a three-chambered heart, there are extensive atrial and interventricular septal defects, due to which the blood mixes twice and enters the systemic and pulmonary circulation. An important pathological sign of all types of congenital heart defects is myocardial hypertrophy; it develops as a result of increased activity of the heart, aimed at compensating for the defects of its development.The weight of the heart with congenital defects exceeds normal on average 1 ‘/ 2–2 times. The greatest weight of the heart is more often observed with defects accompanied by a narrowing of the outflow tract of the right or left ventricles. So, with the tetrad, pentad and triad of Fallot, the weight of the heart reaches 640 g, with a narrowing of the aortic opening – 600 g, with a simultaneous narrowing of the outflow tract of the right and left ventricles – 730 g; with isolated defects of the interventricular or interatrial septa and with non-closure of the botallic duct, the heart weighs an average of 450 g.With congenital heart defects, with the exception of atresia of the right atrioventricular opening and congenital narrowing of the aortic orifice, hypertrophy of the right ventricular myocardium is more pronounced; the myocardium of the left ventricle and the interventricular septum are slightly less hypertrophied, and even less is the atrial myocardium. Thus, regardless of the type of congenital heart disease, all parts of the myocardium are hypertrophied, but mainly that part of it that bears the main severity of the functional load and is the main compensating factor under these conditions of vicious blood circulation.Hypertrophy of the myocardium of heart disease is accompanied by hyperplasia of intramural ethmoid (argyrophilic) fibers. With congenital heart defects, especially if they are accompanied by a narrowing of the arterial cone of the right or left ventricles, small foci of necrosis of muscle fibers and even large myocardial infarctions occur. Severe destructive changes in the myocardium with congenital heart defects in young children develop in the absence of any serious lesions of the coronary arteries of the heart. As myocardial hypertrophy increases, progressive cardiosclerosis develops, focal or diffuse.Separate foci of cardiosclerosis are observed already in infants. The older the patient, i.e. the longer the heart threshold exists, the more pronounced the cardiosclerosis. So, with the most common congenital heart disease of the “blue” type – tetrad of Fallot – diffuse myofibrosis of the right pronounced congestive plethora. Of particular thanatological significance are hemorrhages in the medulla oblongata, which are often not recognized in the clinic and are the cause of death of patients with tetrad, pentad and Fallot triad.Under the influence of hypoxia caused by chronic congestive plethora, dystrophic changes occur in the brain up to the death of nerve cells and the appearance of foci of prolapse. These disorders are most pronounced in the cerebral cortex and in the Purkinje cells of the cerebellum. In the vessels of the lungs with congenital heart defects, the following changes occur: 1) with a decrease in blood filling in the small circle, obliterating processes develop in the pulmonary artery system; 2) increased blood supply to the pulmonary circulation is accompanied by hypertrophic processes in the muscular membrane of the arteries; 3) with a heart defect of the “blue” type, there is one or another degree of development of angomatous structures – additional blood reservoirs; 4) a network of arteriovenous and arterio-arterial anastomoses develops, working in different directions at different indicators of blood pressure in the pulmonary artery; 5) with high degrees of heart defects, destructive processes can occur in arteries of various sizes, incl.hours in arteriovenous anastomoses (plasma impregnation, hyalinosis, wall fibrosis). Based on the data presented, one can get an idea of ​​the morphological changes in the lungs with a given heart defect. For example, during transposition of the great vessels in the lungs, the following develop: hypertrophy of the muscular membrane of the vessels (hypertension in the small circle), angiomatous structures (“blue” defect), arterio-venous anastomoses and destructive changes in the vessels. With an isolated narrowing of the aortic orifice, the following complex of changes in the pulmonary vessels occurs: hypertrophy of the muscular membrane of the vessels (hypertension in the pulmonary circulation) and the development of a network of arterio-venous anastomoses (unloading the pulmonary circulation).With an isolated narrowing of the orifice of the pulmonary artery, obltering processes in the pulmonary artery system (insufficient blood flow and a decrease in pressure in the pulmonary circulation) and the development of arterio-venous anastomoses (compensation for decreased blood flow in the pulmonary artery) come to the fore. With Fallot’s tetrad, there can be a combination of all the above changes (DS Sarkpsov and LD Krymsky). At the same time, changes in the vessels of the lungs are especially difficult for those close to him with heart defects. On the one hand, destructive changes in the vessels and obltering processes in the pulmonary artery system progress, which are expressed in the “recalibration” of the vessels, either in the form of “fixing” their formed folds, then in the growth of the inner shell, then in the formation of “multilateral” vessels.On the other hand, neoplasm of blood vessels is no less pronounced, contributing to the enrichment of the lungs with blood and thereby overcoming chronic oxygen deficiency. At the same time, there is a huge number of newly formed vessels in the connective tissue layers and around the bronchi, a rich network of arteriovenous and arterio-arterial anastomoses and multiple cavernous vascular blood reservoirs, which are a further stage of transformation of “multilateral” vessels. It is possible that the continuous change in the relationship between the processes of obliteration and neoplasm of blood vessels explains the fact that cyanosis in such patients can periodically increase and decrease.It is also possible that the development of a powerful collateral vascular network, in particular “compensatory hemangiomas”, is one of the factors that determine the cases of the existence of Fallot’s tetrad of the “white” type known in the clinic. In postmortem examination, it is necessary to distinguish between changes in organs and systems that were present in patients with congenital heart defects before surgery, from changes that occurred after, as well as as a result of surgery. In this case, significant difficulties can be encountered due to the fact that sometimes a long time passes after the surgical intervention.The lethal outcome in congenital heart defects can be caused by the following main factors: 1) severe disorders of hemo- and cerebrospinal fluid dynamics in the brain; 2) decompensation of a hypertrophied sclerosed heart; 3) respiratory failure that arose after and as a result of surgery; 4) defects in surgery. The most common cause of death in patients with congenital heart defects (especially of the “blue” type) is severe hemo- and CSF dynamics, as well as dystrophic changes in the brain.The next most frequent is decompensation of a hypertrophied heart, sometimes leading to cerebral insufficiency after heart surgery in patients with congenital defects with symptoms of diffuse myofibrosis. However, a strict differentiation of the causes of death in congenital defects according to the predominant changes in the heart, brain and lungs seems to be largely artificial. Clinical presentation and treatment Classification. In clinical practice, congenital heart defects are divided primarily, depending on the presence or absence of arterial hypoxemia, into “cyanotic” (“blue”) and “white” defects, as well as on the state of blood circulation in the pulmonary artery system.Convenient for clinical use is the Marder classification, revised by P.A. Kupriyanov and colleagues According to this classification, congenital heart defects are divided into groups according to the main feature – hemodynamic disturbances in the pulmonary circulation, taking into account the presence or absence of cyanosis. I. Congenital heart defects with increased blood flow through the lungs. chest, developing mainly with an early, pronounced increase in the right ventricle. Hypertension in the pulmonary circulation develops in patients with various types of heart defects, if due to hemodynamic disorders through the vessels of the pulmonary blood flow is increased against the norm.The increase in blood flow is due to the flow of additional amount of arterial blood either from the left half of the heart to the right, or from the aorta to the pulmonary artery (defects of the septum of the heart, open botallic duct). Hypertension is associated with sclerosis and pulmonary vasospasm and is caused by increased resistance in them. Depending on the increase in resistance, the pressure in the pulmonary artery and right ventricle increases. There are four stages (forms) of pulmonary hypertension: 1) mild (initial form) – the pressure in the pulmonary artery is increased to 40 mm Hg.Art .; 2) pronounced – the pressure in the pulmonary artery is increased from 40 to 70 mm Hg. Art .; patients note a sharp shortness of breath that appears during physical exertion; 3) severe – the pressure in the pulmonary artery is increased from 70 to 100 mm Hg. Art .; the amount of blood discharge from the arterial bed to the venous bed decreases; 4) terminal – the pressure in the pulmonary artery system due to pronounced resistance from the vessels of the pulmonary circulation becomes higher than in the aorta; this causes a change in the direction of discharge through a defect in the septum or through an open duct of botal and the development of arterial hypoxemia.A number of authors designate this form as the Eisenmenger symptom complex. The listed general symptoms can be observed with various congenital heart defects. Determination of the type of defect is possible only with a thorough comprehensive clinical and radiological examination of patients using, according to indications, special research methods: angiocardiography, selective angiocardiography, heart sounding and aortography.

      Anatomy of the human heart. Simple and affordable

      The heart is one of the most romantic and sensual organs of the human body.In many cultures, it is considered the seat of the soul, the place where attachment and love originate. However, from an anatomical point of view, the picture looks more prosaic. A healthy heart is a strong muscular organ about the size of its owner’s fist. The work of the heart muscle does not stop for a second from the moment a person is born and until death. By pumping blood, the heart supplies oxygen to all organs and tissues, helps to remove decay products and performs part of the body’s cleansing functions.Let’s talk about the features of the anatomical structure of this amazing organ.

      Cardiology – the science that studies the structure of the heart and blood vessels – was singled out as a separate branch of anatomy back in 1628, when Harvey identified and presented to the medical community the laws of human blood circulation. He demonstrated how the heart, like a pump, pushes blood along the vascular bed in a strictly defined direction, supplying organs with nutrients and oxygen.

      The heart is located in the thoracic region of a person, slightly to the left of the central axis.The shape of the organ can vary depending on the individual characteristics of the structure of the body, age, constitution, sex and other factors. So, in stout, short people, the heart is more rounded than that of thin and tall people. It is believed that its shape roughly matches the circumference of a tightly clenched fist, and its weight ranges from 210 grams for women to 380 grams for men.

      The volume of blood pumped by the heart muscle per day is about 7-10 thousand liters, and this work is carried out continuously! The amount of blood can vary due to physical and psychological conditions.Under stress, when the body needs oxygen, the load on the heart increases significantly: at such moments it is able to move blood at a speed of up to 30 liters per minute, restoring the body’s reserves. Nevertheless, the organ is not able to constantly work for wear and tear: at rest moments, the blood flow slows down to 5 liters per minute, and the muscle cells that form the heart rest and recover.

      The heart is classified as a muscle, however, it is erroneous to believe that it consists of only muscle fibers.The wall of the heart includes three layers, each of which has its own characteristics:

      1. Endocardium is the inner sheath that lines the surface of the chambers. It is represented by a balanced symbiosis of elastic connective and smooth muscle cells. It is almost impossible to outline the clear boundaries of the endocardium: thinning, it smoothly passes into the adjacent blood vessels, and in especially thin places of the atria fuses directly with the epicardium, bypassing the middle, most extensive layer – the myocardium.

      2. Myocardium is the muscular frame of the heart. Several layers of striated muscle tissue are connected in such a way as to quickly and purposefully respond to arousal that occurs in one area and passes through the entire organ, pushing blood into the vascular bed. In addition to muscle cells, the myocardium contains P-cells that are capable of transmitting nerve impulses. The degree of development of the myocardium in certain areas depends on the volume of functions assigned to it. For example, the myocardium in the atrium is much thinner than the ventricular.

      In the same layer is the annulus fibrosus, which anatomically separates the atria and ventricles. This feature allows the chambers to contract alternately, pushing blood in a strictly defined direction.

      3. Epicardium – the superficial layer of the heart wall. The serous membrane, formed by the epithelial and connective tissue, is an intermediate link between the organ and the heart sac – the pericardium. The thin transparent structure protects the heart from increased friction and facilitates the interaction of the muscle layer with adjacent tissues.

      Outside, the heart is surrounded by the pericardium – a mucous membrane that is otherwise called a heart bag. It consists of two sheets – the outer one, facing the diaphragm, and the inner one, tightly fitting to the heart. Between them is a fluid-filled cavity that reduces friction during heartbeats.

      The heart cavity is divided into 4 sections:

      • right atrium and ventricle filled with venous blood;
      • Left atrium and ventricle with arterial blood.

      The right and left halves are separated by a dense septum, which prevents the two types of blood from mixing and maintains unilateral blood flow. True, this feature has one small exception: in children in the womb, there is an oval window in the septum, through which blood is mixed in the heart cavity. Normally, at birth, this hole is overgrown and the cardiovascular system functions as in an adult. Incomplete closure of the oval window is considered a serious pathology and requires surgical intervention.

      Between the atria and the ventricles, the mitral and tricuspid valves are located in pairs, which are held in place by tendon threads. Synchronous contraction of the valves allows unilateral blood flow, preventing mixing of arterial and venous flow.

      The largest artery of the bloodstream, the aorta, departs from the left ventricle, and the pulmonary trunk originates in the right ventricle. In order for the blood to move exclusively in one direction, there are semilunar valves between the chambers of the heart and the arteries.

      The blood flow is ensured by the venous network. The inferior vena cava and one superior vena cava flow into the right atrium, and the pulmonary veins, respectively, into the left.

      Since the supply of oxygen and nutrients to other organs directly depends on the normal functioning of the heart, it must ideally adapt to changing environmental conditions, working in a different frequency range.Such variability is possible due to the anatomical and physiological characteristics of the heart muscle:

      1. Autonomy implies complete independence from the central nervous system. The heart contracts from impulses produced by itself, so the work of the central nervous system does not affect the heart rate in any way.
      2. Conduction is the transmission of the generated impulse along the chain to other parts and cells of the heart.
      3. Excitability implies an immediate response to changes in the body and outside it.
      4. Contractility, that is, the force of contraction of fibers, directly proportional to their length.
      5. Refractoriness is the period during which myocardial tissue is not excitable.

      Any failure in this system can lead to a sharp and uncontrolled change in heart rate, asynchrony of heart contractions, up to fibrillation and death.

      In order to continuously move blood through the vessels, the heart must contract.Based on the stage of contraction, there are 3 phases of the cardiac cycle:

      • Atrial systole, during which blood flows from the atria to the ventricles. In order not to interfere with the current, the mitral and tricuspid valves open at this moment, and the semilunar ones, on the contrary, close.
      • Ventricular systole refers to the movement of blood further to the arteries through the open semilunar valves. This closes the flap valves.
      • Diastole involves filling the atria with venous blood through open leaflet valves.

      Each heartbeat lasts about one second, but with active physical work or during stress, the speed of the impulses increases by shortening the duration of diastole. During good rest, sleep or meditation, heartbeats, on the contrary, slow down, diastole becomes longer, so the body is more actively cleared of metabolites.

      In order to fully perform the assigned functions, the heart must not only pump blood throughout the body, but also receive nutrients from the bloodstream itself.The aortic system, which carries blood to the muscle fibers of the heart, is called the coronary system and includes two arteries – left and right. Both of them move away from the aorta and, moving in the opposite direction, saturate the heart cells with useful substances and oxygen contained in the blood.

      Cardiac muscle conduction system

      Continuous contraction of the heart is achieved due to its autonomous work. An electrical impulse that triggers the process of contraction of muscle fibers is generated in the sinus node of the right atrium at a frequency of 50–80 pulses per minute.Along the nerve fibers of the atrioventricular node, it is transmitted to the interventricular septum, then along large bundles (His legs) to the walls of the ventricles, and then passes to the smaller nerve fibers of Purkinje. Thanks to this, the heart muscle can progressively contract, pushing blood from the internal cavity into the vascular bed.

      The state of the whole organism directly depends on the full functioning of the heart, therefore the goal of any sane person is to maintain the health of the cardiovascular system.In order not to face cardiac pathologies, you should try to exclude or at least minimize provoking factors:

      • overweight;
      • smoking, consumption of alcoholic and narcotic substances;
      • irrational diet, abuse of fatty, fried, salty foods;
      • increased cholesterol level;
      • inactive lifestyle;
      • super-intense physical activity;
      • a state of persistent stress, nervous exhaustion and overwork.

      Knowing a little more about the anatomy of the human heart, try to make an effort on yourself by giving up destructive habits. Change your life for the better, and then your heart will work like a clock.

      .