The heart is a muscular organ found in all vertebrates that is responsible for pumping blood throughout the blood vessels by repeated, rhythmic contractions. The term cardiac (as in cardiology) means "related to the heart" and comes from the Greek καρδιά, kardia, for "heart."
The vertebrate heart is composed of cardiac muscle, which is an involuntary striated muscle tissue found only within this organ. The average human heart, beating at 72 beats per minute, will beat approximately 2.5 billion times during an average 66 year lifespan. It weighs on average 250 g to 300 g in females and 300 g to 350 g in males.
The mammalian heart is derived from embryonic mesoderm germ-layer cells that differentiate after gastrulation into mesothelium, endothelium, and myocardium. Mesothelial pericardium forms the outer lining of the heart. The inner lining of the heart, lymphatic and blood vessels, develop from endothelium. Myocardium develops into heart muscle.
From splanchnopleuric mesoderm tissue, the cardiogenic plate develops cranially and laterally to the neural plate. In the cardiogenic plate, two separate angiogenic cell clusters form on either side of the embryo. Each cell cluster coalesces to form an endocardial tube continuous with a dorsal aorta and a vitteloumbilical vein. As embryonic tissue continues to fold, the two endocardial tubes are pushed into the thoracic cavity, begin to fuse together, and complete the fusing process at approximately 21 days.
The human embryonic heart begins beating at around 21 days after conception, or five weeks after the last normal menstrual period (LMP). The first day of the LMP is normally used to date the start of the gestation (pregnancy). It is unknown how blood in the human embryo circulates for the first 21 days in the absence of a functioning heart. The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (BPM).
The embryonic heart rate (EHR) then accelerates approximately 100 BPM during the first month of beating, peaking at 165-185 BPM during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 BPM per day, or about 10 BPM every three days, which is an increase of 100 BPM in the first month. After 9.1 weeks after the LMP, it decelerates to about 152 BPM (+/-25 BPM) during the 15th week post LMP. After the 15th week, the deceleration slows to an average rate of about 145 (+/-25 BPM) BPM, at term. The regression formula, which describes this acceleration before the embryo reaches 25 mm in crown-rump length, or 9.2 LMP weeks, is: Age in days = EHR(0.3)+6. There is no difference in female and male heart rates before birth.
The structure of the heart varies among the different branches of the animal kingdom. (See Circulatory system.) Cephalopods have two "gill hearts" and one "systemic heart". In vertebrates, the heart lies in the anterior part of the body cavity, dorsal to the gut. It is always surrounded by a pericardium, which is usually a distinct structure, but may be continuous with the peritoneum in jawless and cartilaginous fish. Hagfishes, uniquely among vertebrates, also possess a second heart-like structure in the tail.
The heart is enclosed in a double-walled sac called the pericardium. The superficial part of this sac is called the fibrous pericardium. This sac protects the heart, anchors its surrounding structures, and prevents overfilling of the heart with blood. It is located anterior to the vertebral column and posterior to the sternum. The size of the heart is about the size of a fist and has a mass of between 250 grams and 350 grams. The heart is composed of three layers, all of which are rich with blood vessels. The superficial layer, called the visceral layer, the middle layer, called the myocardium, and the third layer which is called the endocardium. The heart has four chambers, two superior atria and two inferior ventricles. The atria are the receiving chambers and the ventricles are the discharging chambers. The pathway of blood through the heart consists of a pulmonary circuit and a systemic circuit. Blood flows through the heart in one direction, from the atrias to the ventricles, and out of the great arteries, or the aorta for example. This is done by four valves which are the tricuspid atrioventicular valve, the mitral atrioventicular valve, the aortic semilunar valve, and the pulmonary semilunar valve.
Primitive fish have a four-chambered heart; however, the chambers are arranged sequentially so that this primitive heart is quite unlike the four-chambered hearts of mammals and birds. The first chamber is the sinus venosus, which collects de-oxygenated blood, from the body, through the hepatic and cardinal veins. From here, blood flows into the atrium and then to the powerful muscular ventricle where the main pumping action takes place. The fourth and final chamber is the conus arteriosus which contains several valves and sends blood to the ventral aorta. The ventral aorta delivers blood to the gills where it is oxygenated and flows, through the dorsal aorta, into the rest of the body. (In tetrapods, the ventral aorta has divided in two; one half forms the ascending aorta, while the other forms the pulmonary artery).
In the adult fish, the four chambers are not arranged in a straight row but, instead, form an S-shape with the latter two chambers lying above the former two. This relatively simpler pattern is found in cartilaginous fish and in the more primitive ray-finned fish. In teleosts, the conus arteriosus is very small and can more accurately be described as part of the aorta rather than of the heart proper. The conus arteriosus is not present in any amniotes which presumably having been absorbed into the ventricles over the course of evolution. Similarly, while the sinus venosus is present as a vestigial structure in some reptiles and birds, it is otherwise absorbed into the right atrium and is no longer distinguishable.
In amphibians and most reptiles, a double circulatory system is used but the heart is not completely separated into two pumps. The development of the double system is necessitated by the presence of lungs which deliver oxygenated blood directly to the heart.
In living amphibians, the atrium is divided into two separate chambers by the presence of a muscular septum even though there is only a single ventricle. The sinus venosus, which remains large in amphibians but connects only to the right atrium, receives blood from the vena cavae, with the pulmonary vein by-passing it entirely to enter the left atrium.
In the heart of lungfish, the septum extends part-way into the ventricle. This allows for some degree of separation between the de-oxygenated bloodstream destined for the lungs and the oxygenated stream that is delivered to the rest of the body. The absence of such a division in living amphibian species may be at least partly due to the amount of respiration that occurs through the skin in such species; thus, the blood returned to the heart through the vena cavae is, in fact, already partially oxygenated. As a result, there may be less need for a finer division between the two bloodstreams than in lungfish or other tetrapods. Nonetheless, in at least some species of amphibian, the spongy nature of the ventricle seems to maintain more of a separation between the bloodstreams than appears the case at first glance. Furthermore, the conus arteriosus has lost its original valves and contains a spiral valve, instead, that divides it into two parallel parts, thus helping to keep the two bloodstreams separate.
The heart of most reptiles (except for crocodilians; see below) has a similar structure to that of lungfish but, here, the septum is generally much larger. This divides the ventricle into two halves but, because the septum does not reach the whole length of the heart, there is a considerable gap near the openings to the pulmonary artery and the aorta. In practice, however, in the majority of reptilian species, there appears to be little, if any, mixing between the bloodstreams, so the aorta receives, essentially, only oxygenated blood.
Archosaurs, (crocodilians, birds), and mammals show complete separation of the heart into two pumps for a total of four heart chambers; it is thought that the four-chambered heart of archosaurs evolved independently from that of mammals. In crocodilians, there is a small opening, the foramen of Panizza, at the base of the arterial trunks and there is some degree of mixing between the blood in each side of the heart; thus, only in birds and mammals are the two streams of blood - those to the pulmonary and systemic circulations - kept entirely separate by a physical barrier.
In the human body, the heart is usually situated in the middle of the thorax with the largest part of the heart slightly offset to the left, although sometimes it is on the right (see dextrocardia), underneath the sternum. The heart is usually felt to be on the left side because the left heart (left ventricle) is stronger (it pumps to all body parts). The left lung is smaller than the right lung because the heart occupies more of the left hemithorax. The heart is fed by the coronary circulation and is enclosed by a sac known as the pericardium; it is also surrounded by the lungs. The pericardium comprises two parts: the fibrous pericardium, made of dense fibrous connective tissue, and a double membrane structure (parietal and visceral pericardium) containing a serous fluid to reduce friction during heart contractions. The heart is located in the mediastinum, which is the central sub-division of the thoracic cavity. The mediastinum also contains other structures, such as the esophagus and trachea, and is flanked on either side by the right and left pulmonary cavities; these cavities house the lungs.
The apex is the blunt point situated in an inferior (pointing down and left) direction. A stethoscope can be placed directly over the apex so that the beats can be counted. It is located posterior to the 5th intercostal space just medial of the left mid-clavicular line. In normal adults, the mass of the heart is 250-350 g (9-12 oz), or about twice the size of a clenched fist (it is about the size of a clenched fist in children), but an extremely diseased heart can be up to 1000 g (2 lb) in mass due to hypertrophy. It consists of four chambers, the two upper atria and the two lower ventricles.
In mammals, the function of the right side of the heart (see right heart) is to collect de-oxygenated blood, in the right atrium, from the body (via superior and inferior vena cavae) and pump it, via the right ventricle, into the lungs (pulmonary circulation) so that carbon dioxide can be dropped off and oxygen picked up (gas exchange). This happens through the passive process of diffusion. The left side (see left heart) collects oxygenated blood from the lungs into the left atrium. From the left atrium the blood moves to the left ventricle which pumps it out to the body (via the aorta). On both sides, the lower ventricles are thicker and stronger than the upper atria. The muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation.
Starting in the right atrium, the blood flows through the tricuspid valve to the right ventricle. Here, it is pumped out the pulmonary semilunar valve and travels through the pulmonary artery to the lungs. From there, blood flows back through the pulmonary vein to the left atrium. It then travels through the mitral valve to the left ventricle, from where it is pumped through the aortic semilunar valve to the aorta. The aorta forks and the blood is divided between major arteries which supply the upper and lower body. The blood travels in the arteries to the smaller arterioles and then, finally, to the tiny capillaries which feed each cell. The (relatively) deoxygenated blood then travels to the venules, which coalesce into veins, then to the inferior and superior venae cavae and finally back to the right atrium where the process began.
The heart is effectively a syncytium, a meshwork of cardiac muscle cells interconnected by contiguous cytoplasmic bridges. This relates to electrical stimulation of one cell spreading to neighboring cells.
Some cardiac cells are self-excitable, contracting without any signal from the nervous system, even if removed from the heart and placed in culture. Each of these cells have their own intrinsic contraction rhythm. A region of the human heart called the sinoatrial node, or pacemaker, sets the rate and timing at which all cardiac muscle cells contract. The SA node generates electrical impulses, much like those produced by nerve cells. Because cardiac muscle cells are electrically coupled by inter-calated disks between adjacent cells, impulses from the SA node spread rapidly through the walls of the artria, causing both artria to contract in unison. The impulses also pass to another region of specialized cardiac muscle tissue, a relay point called the atrioventricular node, located in the wall between the right artrium and the right ventricle. Here, the impulses are delayed for about 0.1s before spreading to the walls of the ventricle. The delay ensures that the artria empty completely before the ventricles contract. Specialized muscle fibers called Purkinje fibers then conduct the signals to the apex of the heart along and throughout the ventricular walls. The Purkinje fibres form conducting pathways called bundle branches. This entire cycle, a single heart beat, lasts about 0.8 seconds. The impulses generated during the heart cycle produce electrical currents, which are conducted through body fluids to the skin, where they can be detected by electrodes and recorded as an electrocardiogram (ECG or EKG).
The SA node is found in all amniotes but not in more primitive vertebrates. In these animals, the muscles of the heart are relatively continuous and the sinus venosus coordinates the beat which passes in a wave through the remaining chambers. Indeed, since the sinus venosus is incorporated into the right atrium in amniotes, it is likely homologous with the SA node. In teleosts, with their vestigial sinus venosus, the main centre of coordination is, instead, in the atrium. The rate of heartbeat varies enormously between different species, ranging from around 20 beats per minute in codfish to around 600 in hummingbirds.
Cardiac arrest is the sudden cessation of normal heart rhythm which can include a number of pathologies such as tachycardia, an extremely rapid heart beat which prevents the heart from effectively pumping blood, fibrillation, which is an irregular and ineffective heart rhythm, and asystole, which is the cessation of heart rhythm entirely.
Cardiac tamponade is a condition in which the fibrous sac surrounding the heart fills with excess fluid or blood, suppressing the heart's ability to beat properly. Tamponade is treated by pericardiocentesis, the gentle insertion of the needle of a syringe into the pericardial sac (avoiding the heart itself) on an angle, usually from just below the sternum, and gently withdrawing the tamponading fluids.
The valves of the heart were discovered by a physician of the Hippocratean school around the 4th century BC. However, their function was not properly understood then. Because blood pools in the veins after death, arteries look empty. Ancient anatomists assumed they were filled with air and that they were for transport of air.
Philosophers distinguished veins from arteries but thought that the pulse was a property of arteries themselves. Erasistratos observed the arteries that were cut during life bleed. He described the fact to the phenomenon that air escaping from an artery is replaced with blood which entered by very small vessels between veins and arteries. Thus he apparently postulated capillaries but with reversed flow of blood.
The 2nd century AD, Greek physician Galenos (Galen) knew that blood vessels carried blood and identified venous (dark red) and arterial (brighter and thinner) blood, each with distinct and separate functions. Growth and energy were derived from venous blood created in the liver from chyle, while arterial blood gave vitality by containing pneuma (air) and originated in the heart. Blood flowed from both creating organs to all parts of the body where it was consumed and there was no return of blood to the heart or liver. The heart did not pump blood around, the heart's motion sucked blood in during diastole and the blood moved by the pulsation of the arteries themselves.
Galen believed that the arterial blood was created by venous blood passing from the left ventricle to the right through 'pores' in the inter ventricular septum while air passed from the lungs via the pulmonary artery to the left side of the heart. As the arterial blood was created, 'sooty' vapors were created and passed to the lungs, also via the pulmonary artery, to be exhaled.
The first major scientific understanding of the heart was put forth by the medieval Arab polymath Ibn Al-Nafis, regarded as the father of circulatory physiology. He was the first physician to correctly describe pulmonary circulation, the capillary and coronary circulations. Prior to this, Galen's theory was widely accepted, and improved upon by Avicenna. Al-Nafis rejected the Galen-Avicenna theory and corrected many wrong ideas that were put forth by it, and also adding his new found observations of pulse and circulation to the new theory. His major observations include (as surmised by Dr. Paul Ghalioungui):
For more recent technological developments, see Cardiac surgery.
Obesity, high blood pressure, and high cholesterol can increase the risk of developing heart disease. However, fully half the amount of heart attacks occur in people with normal cholesterol levels. Heart disease is a major cause of death (and the number one cause of death in the Western World).
Of course one must also consider other factors such as lifestyle, for instance the amount of exercise one undertakes and their diet, as well as their overall health (mental and social as well as physical).
The Heart has long been used as a symbol to refer to the spiritual, emotional, moral, and in the past also intellectual core of a human being. As the heart was once widely believed to be the seat of the human mind, the word heart continues to be used poetically to refer to the soul, and stylized depictions of hearts are extremely prevalent symbols representing love.
Daphine Rose Kingma Today, see if you can stretch your heart and expand your love so that it touches not only those to whom you can give it easily, but also those who need it so much.
The Institute Of HeartMath and HeartMath LLC have a resource called Heart Quotes. see www.heartquotes.net
HEART, in anatomy. - The heart 1 is a four-chambered muscular bag, which lies in the cavity of the thorax between the two lungs. It is surrounded by another bag, the pericardium, for protective and lubricating purposes (see Coelom And Serous Membranes). Externally the heart is somewhat conical, its base being directed upward, backward and to the right, its apex downward, forward and to the left. In transverse section the cone is flattened, so that there is an anterior and a posterior surface and a superior and inferior border. The superior border, running obliquely downward and to the left, is very thick, and so gains the name of margo obtusus, while the inferior border is horizontal and sharp and is called margo acutus (see fig. I). The divisions between the four chambers of the heart (namely, the two auricles and two ventricles) are indicated on the surface by grooves, and when these are followed it will be seen that the FIG. I. The Thoracic Viscera. - In this diagram the lungs are turned to the side, and the pericardium removed to display the heart. a, upper, a', lower lobe of left lung; b, upper, b', middle, b", lower lobe of right lung; c, trachea; d, arch of aorta; e, superior vena cava; f, pulmonary artery; g, left, and h, right auricle; k, right, and 1, left ventricle; m, inferior vena cava; n, descending aorta; 1, innominate artery; 2, right, and 4, left common carotid artery; 3, right, and 5, left subclavian artery; 6, 6, right and left innominate vein; 7 and 9, left and right internal jugular veins; 8 and 10, left and right subclavian veins; II, 12, 13, left pulmonary artery, bronchus and vein; 14, 15, 16, right pulmonary bronchus, artery and vein; 17 and 18, left and right coronary arteries.
right auricle and ventricle lie on the front and right side, while the left auricle and ventricle are behind and on the left.
The right auricle is situated at the base of the heart, and its outline is seen on looking at the organ from in front. Into the 1 In O. Eng. heorte; this is a common Teut. word, cf. Dut. hart, Ger. Herz, Goth. hairto; related by root are Lat. cor and Gr. Kapbia: the ultimate root is hard-, to quiver, shake.
posterior part of it open the two venae cavae (see fig. 2), the superior (a) above and the inferior (b) below. In front and to the left of the superior vena cava is the right auricular appendage (e) which overlaps the front of the root of the j' aorta, while running obliquely from the front of one vena cava to the other is a shah low groove called the sulcus terminalis, which indicates the original separation between the true auricle in front and the sinus venosus behind. When the auricle is opened by turning the front wall to the right as a flap the following structures are exposed: 1. A muscular ridge, called the crista terminalis, corresponding to the sulcus terminalis on the exterior.
2. A series of ridges on the anterior wall and in the appendage, running downward from the last and at right angles to it, like the teeth of a comb; these are known as musculi pectinati. 3. The orifice of the superior vena cava (fig. 2, a) at the upper and back part of the chamber.
4. The orifice of the inferior vena cava (fig. 2, b) at the lower and back part.
5. Attached to the right and lower margins of this opening are the remains of the Eustachian valve (fig. 2, h), which in the foetus directs the blood from the inferior vena cava, through the foramen ovale, into the left auricle.
6. Below and to the left of this is the opening of the coronary sinus (fig. 2, k), which collects most of the veins returning blood from the substance of the heart.
7. Guarding this opening is the coronary valve or valve of Thebesius. 8. On the posterior or septal wall, between the two auricles, is an oval depression, called the fossa ovalis (fig. 2, g), the remains of the original communication between the two auricles. In about a quarter of all normal hearts there is a small valvular communication between the two auricles in the left margin of this depression (see " 7th Report of the Committee of Collective Investigation," Anat. and Phys. vol. xxxii. p. 164).
9. The annulus ovalis is the raised margin surrounding this depression.
Io. On the left side, opening into the right ventricle, is the right auriculo-ventricular opening. I 1. On the right wall, between the two caval openings, may occasionally be seen a slight eminence, the tubercle of Lower, which is supposed to separate the two streams of blood in the embryo.
12. Scattered all over the auricular wall are minute depressions, the foramina Thebesii, some of which receive small veins from the substance of the heart.
The right ventricle is a triangular cavity (see fig. 2) the base of which is largely formed by the auriculo-ventricular orifice. To the left of this it is continued up into the root of the pulmonary artery, and this part is known as the infundibulum. Its anterior wall forms part of the anterior surface of the heart, while its posterior wall is chiefly formed by the septum ventriculorum, Xiii. 5 Fig. 2. Cavities of the Right Side of the Heart. - a, superior, and b, inferior vena cava; c, arch of aorta; d, pulmonary artery; e, right, and f, left auricular appendage; g, fossa ovalis; h, Eustachian valve; k, mouth of coronary vein; 1, m, n, cusps of the tricuspid valve; o, o, papillary muscles; p, semilunar valve; q, corpus Arantii; r, lunula.
between it and the left ventricle. Its lower border is the margo acutus already mentioned. In transverse section it is crescentic, since the septal wall bulges into its cavity. In its interior the following structures are seen: 1. The tricuspid valve (fig. 2, 1, m, n) guarding against reflux of blood into the right auricle. This consists of a short cylindrical curtain of fibrous tissue, which projects into the ventricle from the margin of the auriculo-ventricular aperture, while from its free edge three triangular flaps hang down, the bases of which touch one another. These cusps are spoken of as septal, marginal and infundibular, from their position.
2. The chordae tendineae are fine fibrous cords which fasten the cusps to the musculi papillares and ventricular wall, and prevent the valve being turned inside out when the ventricle contracts.
3. The columnae carneae are fleshy columns, and are of three kinds. The first are attached to the wall of the ventricle in their whole length and are merely sculptured in relief, as it were; the second are attached by both ends and are free in the middle; while the third are known as the musculi papillares and are attached by one end to the ventricular wall, the other end giving attachment to the chordae tendineae. These musculi papillares are grouped into three bundles (fig. 2, o). 4. The moderator band is really one of the second kind of columnae carneae which stretches from the septal to the anterior wall of the ventricle.
5. The pulmonary valve (fig. 2, p) at the opening of the pulmonary artery has three crescentic, pocket-like cusps, which, when the ventricle is filling, completely close the aperture, but during the contraction of the ventricle fit into three small niches known as the sinuses of Valsalva, and so are quite out of the way of the escaping blood. In the middle of the free margin of each is a small knob called the corpus Arantii (fig. 2, q), and on each side of this a thin crescent-shaped flap, the lunula (fig. 2, r), which is only made of two layers of endocardium, whereas in the rest of the cusp there is a fibrous backing between these two layers.
The left auricle is situated at the back of the base of the heart, behind and to the left of the right auricle. Running down behind it are the oesophagus and the thoracic aorta. When it is opened it is seen to have a much lighter colour than the other cavities, owing to the greater thickness of its endocardium obscuring the red muscle beneath. There are no musculi pectinati except in the auricular appendage. The openings of the four pulmonary veins are placed two on each side of the posterior wall, but sometimes there may be three on the right side, and only one on the left. On the septal wall is a small depression like the mark of a finger-nail, which corresponds to the anterior part of the fossa ovalis and often forms a valvular communication with the right auricle. The auriculo-ventricular orifice is large and oval, and is directed downward and to the left. Foramina Thebesii and venae minimae cordis are found in this auricle, as in the right, although the chamber is one for arterial or oxidized blood.
At the lower part of the posterior surface of the unopened auricle, lying in the left auriculo-ventricular furrow, is the coronary sinus, which receives most of the veins returning the blood from the heart substance; these are the right and left coronary veins at each extremity and the posterior and left cardiac veins from below. One small vein, called the oblique vein of Marshall, runs down into it across the posterior surface of the auricle, from below the left lower pulmonary vein, and is of morphological interest.
The left ventricle is conical, the base being above, behind and to the right, while the apex corresponds to the apex of the heart and lies opposite the fifth intercostal space, 32 in. from the mid line. The following structures are seen inside it: 1. The mitral valve guarding the auriculo-ventricular opening has the same arrangement as the tricuspid, already described, save that there are only two cusps, named marginal and aortic, the latter of which is the larger.
2. The chordae tendineae and columnae carneae resemble those of the right ventricle, though there are only two bundles of musculi papillares instead of three. These are very large. A moderator band has been found as an abnormality (see J. Anat. and Phys. vol. xxx. p. 568).
3. The aortic valve has the same structure as the pulmonary, though the cusps are more massive. From the anterior and left posterior sinuses of; Valsalva the coronary arteries arise. That part of the ventricle just below the aortic valve, corresponding to the infundibulum on the right, is known as the aortic vestibule.
The walls of the left ventricle are three times as thick as those of the right, except at the apex, where they are thinner. The septum ventriculorum is concave towards the left ventricle, so that a transverse section of that cavity is nearly circular. The greater part of it has nearly the same thickness as the rest of the left ventricular wall and is muscular, but a small portion of the upper part is membranous and thin, and is called the pars membranacea septi; it lies between the aortic and pulmonary orifices.
The arrangement of the muscular fibres of the heart is very complicated and only imperfectly known. For details one of the larger manuals, such as Cunningham's Anatomy (London, 1910), or Gray's Anatomy (London, 1909), should be consulted. The general scheme is that there are superficial fibres common to the two auricles and two ventricles and deeper fibres for each cavity. Until recently no fibres had been traced from the auricles to the ventricles, though Gaskell predicted that these would be found, and the credit for first demonstrating them is due to Stanley Kent, their details having subsequently been worked out by W. His, Junr., and S. Tawara. The fibres of this auriculo-ventricular bundle begin, in the right auricle, below the opening of the coronary sinus, and run forward on the right side of the auricular septum, below the fossa ovalis, and close to the auriculo-ventricular septum. Above the septal flap of the tricuspid valve they thicken and divide into two main branches, one on either side of the ventricular septum, which run down to the bases of the anterior and posterior papillary muscles, and so reach the walls of the ventricle, where their secondary branches form the fibres of Purkinje. The bundle is best seen in the hearts of young Ruminants, and it is presumably through it that the wave of contraction passes from the auricles to the ventricles (see article by A. Keith and M. Flack, Lancet, 1 1th of August 1906, p. 359).
The central fibrous body is a triangular mass of fibro-cartilage, situated between the two auriculo-ventricular and the aortic orifices. The upper part of the septum ventriculorum blends with it. The endocardium is a delicate layer of endothelial cells backed by a very thin layer of fibro-elastic tissue; it is continuous with the endothelium of the great vessels and lines the whole of the cavities of the heart.
The heart is roughly about the size of the closed fist and weighs from 8 to 12 oz.; it continues to increase in size up to about fifty years of age, but the increase is more marked in the male than in the female. Each ventricle holds about 4 f. oz. of blood, and each auricle rather less. The nerves of the heart are derived from the vagus, spinal accessory and sympathetic, through the superficial and deep cardiac plexuses.
Embryology. In the article on the arteries (q.v.) the formation and coalescence of the two primitive ventral aortae to form the heart are noticed, so that we may here start with a straight median tube lying ventral to the pharynx and being prolonged cephalad into the ventral aortae and caudad into the vitelline veins. This soon shows four dilatations, which, from the tail towards the head end, are called the sinus venosus, the auricle, the ventricle and the truncus 1 arteriosus. As the tubular heart grows more rapidly than the pericardium which contains it, it becomes bent into the form of an S laid on its side (CD), the ventral convexity being the ventricle and the dorsal the auricle. The passage from the auricle to the ventricle is known as the auricular canal. and in the dorsal and ventral parts of this appear two thickenings 1 This is often called bulbus arteriosus, but it will be seen that the term is used rather differently in comparative anatomy.
known as endocardial cushions, which approach one another and leave a transverse slit between them (fig. 3, E.C.). Eventually these two cushions fuse in the middle line, obliterating the central part of the slit, while the lateral parts remain as the two auriculo-ventricular orifices; this fusion is known as the septum intermedium. From the bottom (ventral convexity) of the ventricle an antero-posterior median septum grows up, which is the septum inferius or septum ventriculorum (fig. 3, V). Posteriorly (caudally) this septum fuses with the septum intermedium, but anteriorly it is free at the lower part of the truncus arteriosus. On referring to the development of the arteries (see Arteries) it will be seen that another septum starts between the last two pairs of aortic arches and grows downward (caudad) until it reaches and joins with the septum inferius just mentioned. This septum aorticum (formed by two ingrowths from the wall of the vessel which fuse later) becomes twisted in such a way that the right ventricle is continuous with the last pair of aortic arches (pulmonary artery), while the left ventricle communicates with the other arches (the permanent ventral aorta and its branches); it joins the septum ventriculorum in the upper part of the ventricular cavity and so forms the pars membranacea septi (fig. 3, T. Ar) .
The fate of the sinus venosus and auricle must now be followed. Into the former, at first, only the two vitelline veins open, but later, as they develop, the ducts of Cuvier acid the umbilical veins join in (see Veins). As the ducts of Cuvier come from each side the sinus spreads out to meet them and becomes transversely elongated. The slight constriction, which at first is the only separation between the sinus and the auricle, becomes more marked, and later the opening is into the right part of the auricle, and is guarded by two valvular folds of endocardium (the venous valves) which project into that cavity, and are continuous above with a temporary downgrowth from the roof, known as the septum spurium. Later the right side of the sinus enlarges, and so does the right part of the aperture, until the back part of the right side of the auricle and the right part of the sinus venosus are thrown into one, and the only remnants of the partition are the crista terminalis and the Eustachian and Thebesian valves. The left part of the sinus venosus, which does not enlarge at the same rate as the right part, remains as the coronary sinus. It will now be seen why, in the adult heart, all the veins which open into the right auricle open into its posterior part, behind the crista terminalis. The septum spurium has been referred to as a temporary structure; the real division between the two auricles occurs at a later date than that between the ventricles and to the left of the septum spurium. It is formed by two partitions, the first of which, called the septum primum, grows down from the auricular roof. At first it does not quite reach the endocardial cushions in the auricular canal, already mentioned, but leaves a gap, called the ostium primum, between. This has nothing to do with the foramen ovale, which occurs as an independent perforation higher up, and at first is known as the ostium secundum. When it is established the septum primum grows down and meets the endocardial cushions, and so the ostium primum is obliterated. The septum secundum grows down on the right of the septum primum and is never complete; it grows round and largely overlaps the foramen ovale and its edges form the annulus ovalis, so that, in the later months of foetal life, the foramen ovale is a valvular opening, the floor of which is formed by the septum primum and the margins by the septum secundum. The closure of the foramen is brought about by adhesion of the two septa.
The pulmonary veins of the two sides at first join one another, dorsal to the left auricle, and open into that cavity by a single median trunk, but, as the auricle grows, this trunk and part of the right and left veins are absorbed into its cavity.
The mitral and tricuspid valves are formed by the shortening of the auricular canal which becomes telescoped into the ventricle, and the cusps are the remnants of this telescoping process.
The columnae carneae and chordae tendineae are the remains of a spongy network which originally filled the cavity of the primary ventricle.
The aortic and pulmonary valves are laid down in the ventral aorta, before it is divided into aorta and pulmonary artery, as four endocardial cushions; anterior, posterior and two lateral. The septum aorticum cuts the latter two into two, so that each artery has the rudiments of three cusps.
Abnormalities of the heart are very numerous, and can usually be explained by a knowledge of its development. They often cause grave clinical symptoms. A clear and well-illustrated review of the most important of them will be found in the chapter on congenital disease of the heart in Clinical Applied Anatomy, by C. R. Box and W. McAdam Eccles, London, 1906.
For further details of the embryology of the heart see Oscar Hertwig's Entwickelungslehre der Wirbeltiere (Jena, 1902); G. Born, " Entwicklung des Sdugetierherzens," Archl y f. mik. Anat. Bd. 33 (1889); W. His, Anatomie menschlicher Embryonen (Leipzig, 188'- 1885); Quain's Anatomy, vol. i. (1908); C. S. Minot, Human Embryology (New York, 1892); and A. Keith, Human Embryology and Morphology (London, 1905).
Comparative Anatomy. In the Acrania (e.g. lancelet) there is no heart, though the vessels are specially contractile in the ventral part of the pharynx.
In the Cyclostomata (lamprey and hag), and Fishes, the heart has the same arrangement which has been noticed in the human embryo. There is a smooth, thin-walled sinus venosus, a thin reticulate-walled auricle, produced laterally into two appendages, a thick-walled ventricle, and a conus arteriosus containing valves. In addition to these the beginning of the ventral aorta is often thickened and expanded to form a bulbus arteriosus, which is non-contractile, and, strictly speaking, should rather be described with the arteries than with the heart. In relation to human embryology the smooth sinus venosus and reticulated auricle are interesting. Between the auricle and ventricle is the auriculo-ventricular valve, which primarily consists of two cusps, comparable to the two endocardial cushions of the human embryo, though in some forms they may be subdivided. In the interior of the ventricle is a network of muscular trabeculae. The conus arteriosus in the Elasmobranchs (sharks and rays) and Ganoids (sturgeon) is large and provided with several rows of semilunar valves, but in the Cyclostomes (lamprey) and Teleosts (bony fishes) the conus is reduced and only the anterior (cephalic) row of valves retained. With the reduction of the conus the bulbus arteriosus is enlarged. So far the heart is a single tubular organ expanded into various cavities and having the characteristic (A-shaped form seen in the human embryo; it contains only venous blood which is forced through the gills to be oxidized on its way to the tissues. In the Dipnoi (mud fish), in which rudimentary lungs, as well as gills, are developed, the auricle is divided into two, and the sinus venosus opens into the right auricle. The conus arteriosus too begins to be divided into two chambers, and in Protopterus this division is complete. This division of the heart is one instance in which mammalian ontogeny does not repeat the processes of phylogeny, because, in the human embryo, it has been shown that the ventricular septum appears before the auricular. This want of harmony is sometimes spoken of as the " falsification of the embryological record." In the Amphibia there are also two auricles and one ventricle, FIG. 3. - Formation of Septa. Diagram of the formation of some of th6 septa of the heart (viewed from the right side). S.V. Sinus venosus.
E.C. Endocardial cushions forming septum intermedium.
V. Septum ventriculorum.
T. Ar. Septum aorticum intruncus arteriosus.
V.A. Ventral aorta.
though in the Urodela (tailed amphibians) the auricular septum is often fenestrated. The sinus venosus is still a separate chamber, and the conus arteriosus, which may contain many or few valves, is usually divided into two by a spiral fold. Structurally the amphibian heart closely resembles the dipnoan, though the increased size of the left auricle is an advance. In the Anura (frogs and toads) the whole ventricle is filled with a spongy network which prevents the arterial and venous blood from the two auricles mixing to any great extent. (For the anatomy and physiology of the frog's heart, see The Frog, by Milnes Marshall.) In the Reptiles the ventricular septum begins to appear; this in the lizards is quite incomplete, but in the crocodiles, which are usually regarded as the highest order of living reptiles, the partition has nearly reached the top of the ventricle, and the condition resembles that of the human embryo before the pars membranacea septi is formed. The conus arteriosus becomes included in the ventricular cavity, but the sinus venosus still remains distinct, and its opening into the right ventricle is guarded by two valves which closely resemble the two venous valves in the auricle of the human embryo already referred to.
In the Birds the auricular and ventricular septa are complete; the right ventricle is thin-walled and crescentic in section, as in Man, and the musculi papillares are developed. The left auriculoventricular valve has three membranous cusps with chordae tendineae attached to them, but the right auriculo-ventricular valve has a large fleshy cusp without chordae tendineae. The sinus venosus is largely included in the right auricle, but remains of the two venous valves are seen on each side of the orifice of the inferior vena cava.
In the Mammals the structure of the heart corresponds closely with the description of that of Man already given. In the Ornithorynchus, among the Monotremes, the right auriculoventricular valve has two fleshy and two membranous cusps, thus showing a resemblance to that of the bird. In the Echidna, the other member of the order, however, both auriculo-ventricular valves are membranous. In the Edentates the remains of the venous valves at the opening of the inferior vena cava are better marked than in other orders. In the Ungulates the moderator band in the right ventricle is especially well developed, and the central fibrous body at the base of the heart is often ossified, forming the os cordis so well known in the heart of the ox.
The position of the heart in the lower mammals is not so oblique as it is in Man.
For further details, see C. Rose, Beitr. z. vergl. Anat. des Herzens der Wirbelthiere Morph. Jahrb., Bd. xvi. (1890); R. Wiedersheim, Vergleichende Anatomie der Wirbelthiere (Jena, 1902) (for literature); also Parker and Haswell's Zoology (London, 1897). (F. G. P.) Heart Disease. - In the early ages of medicine, the absence of correct anatomical, physiological and pathological knowledge prevented diseases of the heart from being recognized with any certainty during life, and almost entirely precluded them from becoming the object of medical treatment. But no sooner did Harvey (1628) publish his discovery of the circulation of the blood, and its dependence on the heart as its central organ, than derangements of the circulation began to be recognized as signs of disease of that central organ. (See also under Vascular System.) Among the earliest to profit by this discovery and to make important contributions to the literature of diseases of the heart and circulation were, R. Lower (1631-1691), R. Vieussens (1641-1716), H. Boerhave (1668-1738) and the great pathologists at the beginning of the 18th century, G. M. Lancisi (1654-1720), G. B. Morgagni (1682-1771) and J. B. Senac (1693-1770). The works of these writers form very interesting reading, and it is remarkable how careful were the observations made, and how sound the conclusions drawn, by these pioneers of scientific medicine. J. N. Corvisart (1755-1821) was one of the earliest to make practical use of R. T. Auenbrugger's (1722-1809) invention of percussion to determine the size of the heart. R. T. H. Laennec (1781-1826) was the first to make a scientific application of mediate auscultation to the diagnosis of disease of the chest, by the invention of the stethoscope. J. Bouillaud (1796-1881) extended its use to the diagnosis of disease of the heart. To James Hope (1801-1841) we owe much of the precision we have now attained in diagnosis of valvular disease from abnormalities in the sounds produced during cardiac movements. This short list by no means exhausts the earlier literature on the subject, but each of these names marks an era in the progress of the diagnosis of cardiac disease. In later years the literature on this subject has become very copious.
The heart and great vessels occupy a position immediately to the left of the centre of the thoracic cavity. The anterior surface of the heart is projected against the chest wall and is surrounded on either side by the lungs, which are resonant organs, so that any increase in the size of the heart, " dilatation," can be detected by percussion. By placing the hand on the chest, palpation, the impulse of the left ventricle, or apex beat, can normally be felt just below and internal to the nipple. Deviations from the normal in the position or force of the apex beat will afford important information as to the nature of the pathological changes in the heart. Thus, displacement downwards and outwards of the apex beat, with a forcible thrusting impulse, will indicate hypertrophy, or increase of the muscular wall and increased driving power of the left ventricle, whereas a similar displacement with a feeble diffuse impulse will indicate dilatation, or over-distension of its cavity from stretching of the walls.
By auscultation, or listening with a suitable instrument named a stethoscope over appropriate areas, we can detect any abnormality in the sounds of the heart, and the presence of murmurs indicative of disease of one or other of the valves of the heart.
The pericardium is a fibro-serous sac which loosely envelops the heart and the origin of the great vessels. Inflammation of this sac, or pericarditis, is apt to occur as a result of rheumatism, more especially in children. It may also occur as a complication of pneumonia. It is a serious affection associated with pain over the heart, fever, shortness of breath, rapid pulse and dilatation of the heart. As a result of the inflammation, fluid may accumulate in the pericardial sac, or the walls of the sac may become adherent to the heart and tend to embarrass its action. In favourable cases, however, recovery may take place without any untoward sequelae.
Diseases of the heart may be classified in two main groups, (I) Disease of the valves, and (2) Disease of the walls of the heart.
1. Valvular Disease. - Inflammation of the valves of the heart, or endocarditis, is one of the most common complications of rheumatism in children and young adults. More severe types, which are apt to prove fatal from a form of blood poisoning, may result when the valves of the heart are attacked by certain micro-organisms, such as the pneumococcus, which is responsible for pneumonia, the streptococcus and the staphylococcus pyogenes, the gonococcus and the influenza bacillus.
As a result of endocarditis, one or more of the valves may be seriously damaged, so that it leaks or becomes incompetent. The valves of the left side of the heart, the aortic and mitral valves, are affected far more commonly than those of the right side. It is indeed comparatively rarely that the latter are attacked. In the process of healing of a damaged valve, scar tissue is formed which has a tendency to contract, so that in some cases the orifice of the valve becomes narrowed, and the resulting stenosis or narrowing gives rise to obstruction of the blood stream. We may thus have incompetence or stenosis of a valve or both combined.
Valvular lesions are detected on auscultation over appropriate areas by the blowing sounds or murmurs to which they give rise, which modify or replace the normal heart sounds. Thus, lesions of the mitral valve give rise to murmurs which are heard at the apex beat of the heart, and lesions of the aortic valves to murmurs which are heard over the aortic area, in the second right intercostal space. Accurate timing of the murmurs in relation to the heart sounds enables us to judge whether the murmur is due to stenosis or incompetence of the valve affected.
If the valvular lesion is severe, it is essential for the proper maintenance of the circulation that certain changes should take place in the heart to compensate for or neutralize the effects of the regurgitation or obstruction, as the case may be. In affections of the aortic valve, the extra work falls on the left ventricle, which enlarges proportionately and undergoes hypertrophy. In affections of the mitral valve the effect is felt primarily by the leftauricle, which is a thin walled structure incapable of undergoing the requisite increase in power to resist the backward flow through the mitral orifice in case of leakage, or to overcome the effects of obstruction in case of stenosis. The back pressure is therefore transmitted to the pulmonary circulation, and as the right ventricle is responsible for maintaining the flow of blood through the lungs, the strain and extra work fall on the right ventricle, which in turn enlarges and undergoes hypertrophy. The degree of hypertrophy of the left or right ventricle is thus, up to a certain point, a measure of the extent of the lesion of the aortic or mitral valve respectively. When the effects of the valvular lesion are so neutralized by these structural changes in the heart that the circulation is equably maintained, " compensation " is said to be efficient.
When the heart gives way under the strain, compensation is said to break down, and dropsy, shortness of breath, cough and cyanosis, are among the distressing symptoms which may set in. The mere existence of a valvular lesion does not call for any special treatment so long as compensation is efficient, and a large number of people with slight valvular lesions are living lives indistinguishable from those of their neighbours. It will, however, be readily understood that in the case of the more serious lesions certain precautions should be observed in regard to over-exertion, excitement, over-indulgence in tobacco or alcohol, &c., as the balance is more readily upset and any undue strain on the heart may cause a breakdown of compensation. When this occurs treatment is required. A period of rest in bed is often sufficient to enable the heart to recover, and this may be supplemented as required by the administration of mercurial and saline purgatives to relieve the embarrassed circulation, and of suitable cardiac tonics, such as digitalis and strychnin, to reinforce and strengthen the heart's action.
2. Affections of the Muscular Wall of the Heart. - Dilatation of the heart, or stretching of the walls of the heart, is an incident, as has already been stated, in pericarditis and in the earlier stages of valvular disease antecedent to hypertrophy. Temporary over-distension or dilatation of the cavities of the heart occurs in violent and protracted exertion, but rapidly subsides and is in no wise harmful to the sound and vigorous heart of the young. It is otherwise if the heart is weak and flabby from a too sedentary life or degenerative changes in its walls or during convalescence from a severe illness, when the same circumstances which will not injure a healthy heart, may give rise to serious dilatation from which recovery may be very protracted.
Influenza is a common cause of cardiac dilatation, and is liable to be a source of trouble after the acute illness has subsided, if the patient goes about and resumes his ordinary avocations too soon.
Fatty or fibroid degeneration of the heart wall may occur in later life from impaired nutrition of the muscle, due to partial obstruction of the blood-vessels supplying it, when they are the seat of the degenerative changes known as arteriosclerosis or atheroma. The affection known as angina pectoris (q.v.) may be a further consequence of this defective blood-supply.
The treatment will vary according to the nature of the case. In serious cases of dilatation, rest in bed, purgatives and cardiac tonics may be required.
In commencing degenerative change the Oertel treatment, consisting of graduated exercise up a gentle slope, limitation of fluids and a special diet, may be indicated.
In cases of slight dilatation after influenza or recent illness, the Schott treatment by baths and exercises as carried out at Nauheim ma " be sometimes beneficial. The change of air and scene, the enforced rest, the placid life, together with freedom from excitement and worry, are among the most important factors which contribute to success in this class of case. Disorders of Rhythm of the Heart's Action. - Under this heading may be grouped a number of conditions to which the name " functional affections of the heart "has sometimes been applied, inasmuch as the disturbances in question cannot usually be attributed to definite organic disease of the heart. We must, of course, exclude from this category the irregularity in the force and frequency of the pulse, which is commonly associated with incompetence of the mitral valve.
The heart is a muscular organ possessing certain properties, rhythmicity, excitability, contractility, conductivity and tonicity, as pointed out by Gaskell, in virtue of which it is able to maintain a regular automatic beat independently of nerve stimulation. It is, however, intimately connected with the brain, blood-vessels and the abdominal and thoracic viscera, by innumerable nerves, through which impulses or messages are being constantly sent to and received from these various portions of the body. Such messages may give rise to disturbances of rhythm with which we are all familiar. For instance, sudden fright or emotion may cause a momentary arrest of the heart's action, and excitement or apprehension may set up a rapid action of the heart or palpitation. Palpitation, again, is often the result of digestive disorders, the message in this case being received from the stomach, instead of the brain as in emotional disturbances. It may also result from over-indulgence in tobacco and alcohol.
Tachycardia is the name applied to a more or less permanent increase in the rate of the heart-beat. It is usually a prominent feature in the affection known as Graves' disease or exophthalmic goitre. It may also result from chronic alcoholism. In the condition known as paroxysmal tachycardia there appears to be no adequate explanation for its onset.
Bradycardia or abnormal slowness of the heart-beat, is the converse of tachycardia. An abnormally slow pulse is met with in melancholia, cerebral tumour, jaundice and certain toxic conditions, or may follow an attack of influenza. There is, however, a peculiar affection characterized by abnormal slowness of pulse (often ranging as low as 30), and the onset, from time to time, of epileptiform or syncopal attacks. To this the name " Stokes-Adams disease " has been applied, as it was first called attention to by Adams in 1827, and subsequently fully described by Stokes in 1836. It is usually associated with senile degenerative change of the heart and vascular system, and is held to be due to impairment of conductivity in the muscular fibres (bundle of His) which transmit the wave of contraction from the auricle to the ventricle. It is of serious significance in view of the symptoms associated with it.
By this is understood a pulse in which a beat is dropped from time to time. The dropping of a beat may occur at regular intervals every two, four or six beats, &c., or occasionally at irregular intervals after a series of normal beats. On examining the heart, it is found, as a rule, that the cause of the intermission at the wrist is not actual omission of a heart-beat, but the occurrence of a hurried imperfect cardiac contraction which does not transmit a pulse-wave to the wrist. It is not characteristic of any special form of heart affection, and is rarely of serious import. It may be due to reflex digestive disturbances, or be associated with conditions of nervous breakdown and irritability, or with an atonic and relaxed condition of the heart muscle. The treatment of these disorders of rhythm of the heart will vary greatly according to the cause and is often a matter of considerable difficulty. (J. F. H. B.) Surgery of Heart and Pericardium. - As the result of acute or chronic inflammation of the lining membrane of the fibrous sac which surrounds the heart and the neighbouring parts of the large blood-vessels, a dropsical or a purulent collection may form in it, or the sac may be quietly distended by a thin watery fluid. In, either case, but especially in the latter, the heart may be so embarrassed in its work that death seems imminent. The condition is generally due to the cultivation in the pericardium of the germs of rheumatism, influenza or gonorrhoea, or of those of ordinary suppuration. Respiration as well as circulation is embarrassed, and there is a marked fulness and dulness of the front wall of the chest to the left of the breast-bone. In that region also pain and tenderness are complained of. By using the slender, hollow needle of an aspirator great relief may be afforded, but the tapping may have to be repeated from time to time. If the fluid drawn off is found to be purulent, it may be necessary to make a trap-door opening into the chest by cutting across the 4th and 5th ribs, incising and evacuating the pericardium and providing for drainage. In short, an abscess in the pericardium must be treated like an abscess in the pleura.
Wounds of the heart are apt to be quickly fatal. If the probability is that the enfeebled action of the heart is due to pressure from blood which is leaking into, and is locked up in the pericardium, the proper treatment will be to open the pericardium, as described above, and, if possible, to close the opening in the auricle, ventricle or large vessel, by sutures. (E. 0.*).
Procedures of Tissue Preparation | Glossary | Resources
Ep.: 1:100 Neugeborene
Herzfehler mit Links-rechts-Shunt ohne Zyanose und hyperkinetisch bedingter pulmonaler Hypertonie und Überdurchblutung der Lunge.
Der physiologische Verschluss nach der Geburt unterbleibt.
Folge: Kontinuierlicher (Windkessel!) Links-rechts-Shunt
Es gibt zwei verschiedene ASDs, die sich aus der Embryologie erklären. Am Anfang sind beide Vorhöfe über das Foramen primum offen verbunden. Das Septum primum wächst von oben Richtung Herzskelett (Klappenebene) herunter und fusioniert dort mit einem Endokardkissen. Eine Störung dieser Fusion führt direkt über den Klappen zum offen Foramen primum, das in seiner vollen Ausprägung dem Atrioventrikulären Septumdefekt (AVSD) entspricht. Einen partieller AVSD (PAVSD) nennt man auch ASD I. Diese Fehlbildung ist häufig bei Trisomie 21 anzutreffen. Die Fehlbildung ist mit weiteren Störungen assoziiert, z.B. Reizleitungsstörungen durch Fehlentwicklung des Reizleitungssystems und einem fehlenden Sprung zwischen Mitral- und Trikuspidalebene.
Das heruntergewachsene Septum primum reisst normalerweise in der Mitte ein und bildet das Foramen secundum bzw. Foramen ovale. Dieses wird durch das links vom Septum primum ebenfalls von oben herunterwachsende Septum secundum gardinenartig bedeckt (Ventil) und kurz nach der Geburt durch Umkehr der Druckverhältnisse funktionell (z.T. strukturell durch Verklebung) verschlossen. Ist der Verschluss so ungenügend, dass es zum Links-rechts-Shunt kommt, spricht man vom offenen Foramen ovale bzw. ASD II. Der ASD II ist im Ggs. zum ASD I weiter oben lokalisiert. Er macht oft wenig Symptome und wird oft erst im Erwachsenenalter erkannt. Der Links-Rechts-Shunt kann im EKG zu Zeichen der Rechtsherzbelastung führen (Rechtslagetyp, P pulmonale, inkompletter Rechtsschenkelblock ohne Hypertrophie-Zeichen (rsr's') als Zeichen der rechtsventrikulären Volumenbelastung) und bei starker Ausprägung zu klinischen Symptomen führen.
Makro: Loch im Kammerseptum, meist im membranösen Teil.
Makro: Fehlende Trennung von Aorta und A. pulmonalis, oft 4-segelige Taschenklappe.
Makro: Partielles Fehlen von Vorhof- und Ventrikelwand (siehe ASD I).
Herzfehler mit Rechts-links-Shunt und dadurch Ausbildung einer Zyanose
Die Fallotsche Tetralogie ist ein komplexer Herzfehler mit einer
Klinik: Die Zyanose tritt erst einige Wochen nach der Geburt auf, da die Lunge pränatal kaum durchblutet ist und der rechte Ventrikel erst nach der Geburt belastet wird und hypertrophiert. Die Hypertrophie verstärkt im circulus vitiosus zunehmend die muskuläre Obstruktion des rechtsventrikulären Ausflusstraktes. Die Klinik der Obstruktion tritt dabei anfallsartig in Form „hypoxämischer Anfälle“ auf. Wenn unbehandelt, nimmt das Kind später im Anfall automatisch eine typische Hockstellung ein, um den venösen Rückfluss zu hemmen und das Herz zu entlasten. Auskultatorisch fällt das pulmonale Stenosegeräusch auf. Der VSD erzeugt wegen dem Druckausgleich zwischen linker und rechter Kammer kaum Turbulenzen und ist daher kaum zu hören.
Makro: Die Aorta ist - inklusive der Koronarien - mit dem rechten, die Pulmonalis mit dem linken Ventrikel verbunden. Die Kreisläufe sind nicht seriell sondern parallel geschaltet. Die periphere Sauerstoffversorgung kann sich nach der Geburt sehr rasch und lebensbedrohlich verschlechtern durch Verschluss der embryonalen Kurzschlüsse (Foramen ovale, Ductus arteriosus BOTALLI).
Klinik: Hyperaktives Präkordium, Zyanose
Makro: Verengung des pulmonalen Ausflusstraktes. Bei relevanter Druckbelastung entwickelt sich eine Rechtsherzhypertrophie.
Makro: Sub-, supra- oder valvuläre Stenose der Aorta aszendens. Folge ist eine Linksherzhypertrophie durch Druckbelastung.
Makro: Es handelt sich um eine hinter dem Abgang der linken A. subclavia gelegene Verengung der Aorta.
Es gibt zwei Formen:
Klinik der infantilen Form: Die Kinder sind bei Geburt typischerweise "gesund" (und passieren oft auch unbemerkt die U2), da die Stenose durch den offenen Ductus arteriosus umgangen wird und auskultatorisch kaum etwas zu hören ist. Die Femoralispulse sind allerdings häufig schon abgeschwächt und ihre Palpation ist die wichtigste diagnostische Maßnahme! Nach etwa 10 bis 14 Tagen entwickeln die Kinder durch den Verschluß des Ductus arteriosus unspezifische Symptome der Linksherzinsuffizienz wie Tachypnoe, Gewichtszunahme (kaum sicht- oder hörbare Ödeme) und Symptome der peripheren Minderperfusion wie Oligurie/Anurie, Trinkschwäche, Verlängerung der Rekapillarisierungszeit, kühle untere Extremitäten. Die Kinder können dann sehr rasch am - im Grunde vermeidbaren - Herzversagen sterben. In diesem Stadium erkannte Kinder müssen sofort notfallmässig behandelt werden, um sie zu retten.
Makro: Hypotrophie des linken Herzens, defekte Mitral- und Aortenklappe
Makro: Die Pulmonalvenen erreichen nicht das linke Atrium, sondern die Portalvene (Pulmonalvene -> Portalvene -> Leber -> V. cava inferior -> rechter Vorhof -> Foramen ovale und Ductus Botalli -> Körperkreislauf -> Lunge) oder den Sinus coronarius.
Makro: Atrialisierter Ventrikel (tiefsitzende Trikuspidalklappen), Trikuspidaldefekt.
Ät.: Degenerativ, rheumatisch
Makro: Die Taschenklappen sind plump verdickt, verkalkt und fusioniert. Die Querschnittsfläche ist verkleinert (< 2,5 cm²).
Klinik: Leistungsminderung, Belastungsdyspnoe, Synkopen, Schwindel.
Kompl.: Bakterielle Endokarditis, KHK (konzentrische Druckhypertrophie des Myokards mit relativer Koronarinsuffizienz), Linksherzinsuffizienz (-> Lungenstauung, Lungenödem),.
Klinik: Leistungsminderung durch die diastolische Füllungsstörung mit Reduktion des Herzzeitvolumens (HZV), Belastungsdyspnoe, spät: Facies mitralis („rote Bäckchen“), periphere Zyanose, Zeichen der Rechtsherzinsuffizienz, Tachyarrhythmia absoluta bei Vorhofflimmern.
Kompl.: Vorhofdilatation mit Vorhofflimmern und evtl. Vorhofthrombose und Embolie, Rückstau in die Lunge (Lungenstauung, Lungenödem) und ggf. bis in den großen Kreislauf (pulmonale Hypertonie, Rechtsherzbelastung/Cor pulmonale, Rechtsherzinsuffizienz), bakterielle Endokarditis.
Ät.: Aufbrechen und/oder Thrombosierung einer arteriosklerotischen Plaque in einer Coronararterie, selten thrombembolischer Verschluß.
Der Myokardinfarkt muss mind. 6 - 12 Stunden überlebt werden, bevor er morphologisch sichtbar wird!
Mikro: Koagulationsnekrose, Einblutungen. Die Myozyten zeigen eine verstärkte Eosinophilie und Kontraktionsbanden quer durch die Herzmuskelfasern. Typische Zellparameter wie Querstreifung, Zellkerne und Zellgrenzen gehen verloren. Das Infarktareal wird von einer Hyperämischen/hämorrhagischen Randzone begrenzt. Im Verlauf zunehmende leukozytäre Demarkation und Phagozytose des nekrotischen Gewebes, sowie Einwanderung von Fibroblasten mit Ausbildung eines narbigen Ersatzgewebes.
Makro: Lehmfarbene Abblassung mit hyperämischem/hämorrhagischem Randsaum.
Kompl.: Herzwandruptur mit Perikardtamponade (i.d.R. zwischen dem 3. und 10. Tag), Herzwandaneurysma, Papillarmuskelnekrose mit Sehnenfadenabriß, Herzrhythmusstörungen, Re-Infarkt, Herzinsuffizienz.
Labor: Positives Troponin T (Schnelltest!), EKG: Anstieg der T-Welle, dann der ST-Strecke.
Mikro: Bindegewebige Narben, Fibrozyten mit z.T. großen ovalen Zellkernen. Kompensatorische Hypertrophie der umgebenden Myozyten. Gute Darstellung in der EVG-Färbung: Herzmuskel grau, Narbe violett.
Makro: Fibrosiertes Areal mit Lipomatosis cordis.
EKG: Negative Q-Zacke
Entzündung der Herzinnenwand und Herzklappen.
Ät.: Endothelschaden + Thrombozytenaggregate + Bakteriämie
RF.: Kardial: Implantate, Herzfehler (-> Jet-Läsionen), Z.n. rheumatischer Endokarditis, Klappenfehler u.a.m., systemisch: Diabetes mellitus, Alkoholabusus, Leberzirrhose, Immundefizite, Hypertonus.
Lok.: Meist sind die mechanisch stärker belasteten Klappen des linken Herzens betroffen
Ät.: Eindringen von Bakterien (Pilzen) in die Blutbahn
Erreger: Staphylococcus aureus, Streptokokken, Gonokokken, Enterokokken, Pilze
Mikro: Fibrin, Plättchen, Bakterienkolonien, Immunzellen
Makro: Große, rötliche, unregelmäßige, brüchige, ulzerierende, polypöse Vegetationen an den Klappen, Ausbreitungstendenz und Klappendestruktion, Splitterhämorrhagien an den Nägeln (septische Mikroembolien).
Kompl.: Sehnenfadenabriß, Klappeninsuffizienz, septische Embolie, z.B. in Herz, Niere und Gehirn (Metastatische Herdenzephalitis), mykotisches Aneurysma (metastatische Absiedelung -> Zerstörung der Gefäßwand -> Aussackung), Immunkomplexvaskultis (Niere: LÖHLEIN-Herdnephritis, Haut: OSLER-Knötchen).
Klinik: Fieber, kutane und konjunktivale petechiale Blutungen, Janeway-Läsionen (palmare/plantare indolente makulöse Hautläsionen), schmerzhafte OSLER-Knötchen palmar/plantar oder an den Fingerkuppen. Mikroembolien an den Akren oder auch subungual (Splitterhämorrhagien). Pathologisches Herzgeräusch (nicht selten das erste Symptom!). Im Verlauf Symptome durch Klappeninsuffizienz, Sehnenfadenabriß, septische Komplikationen.
Prg.: Abh. von der Größe der Vegetationen und dem Erreger (Streptokokken günstiger, Enterokokken ungünstiger, Staphylokokken noch ungünstiger).
Erreger: Streptococcus viridans-Gruppe (Zahnschäden, Parodontitis!), Enterokokken, Cardiobacterium hominis
RF: Ansiedelung auf vorgeschädigten Herzklappen
Verlauf: oft subklinisch, da Erreger weniger virulent
Morph.: ähnlich der akuten Form
|thumb|Subakute Endokarditis durch Haemophilus parainfluenzae.|
Ät.: Häufig bei i.v.-Drogenabusus
Syn.: Endocarditis verrucosa simplex, Endocarditis marantica
Ät.: Chronische, aufzehrende Erkrankungen, Hyperkoagulabilität, DIC, Schock, paraneoplastisch.
Makro: kleine (meist < 5 mm), rosa, wärzchenförmige Vegetationen an den Schließungsrändern der Aorten- und Mitralklappe.
Ät.: Rheumatisches Fieber nach Infekt mit ß-hämolysierenden Streptokokken (Angina tonsillaris, Impetigo)
Makro: 1 - 3 mm kleine, entlang des Klappenschließungsrandes fest haftende Wärzchen, ASCHOFF-Knötchen, immer Pankarditis.
Kompl.: Klappenvitium, z.B. Mitralklappeninsuffizienz
Ät.: Systemischer Lupus erythematodes (SLE)
Makro: Flache, blasse, spreitende Vegetationen auf Klappen, Endokard und Chordae tendineae.
Mikro: Zentral Bakterienkolonien in der Kapillare umsäumt von Immunozyten.
Makro: Kleine, gelbe, punktförmige Mikroabszesse.
Ät.: Coxsackie-, ECHO-, Adenoviren, Influenzaviren
Pathogenese: Herzmuskelnekrose durch Virus und T-Zell-vermittelte Immunreaktion.
Mikro: Interstitielles lymphozytäres Infiltrat (kleine blaue Zellen), kaum Nekrosen.
Ät.: Trypanosoma cruzi (Protozoon, CHAGAS-Krankheit)
2-3 Wochen nach Infektion (Tonsillitis, Tbc, Diphterie), der betreffende Erreger ist nicht nachweisbar.
Ät.: Rheumatisches Fieber, infektallergisch, i.R. systemischer Viruserkrankungen.
Mikro: Granulomatöse Entzündung, ASCHOFF Knötchen perivasal (ASCHOFF Riesenzellen: Große, ein- oder mehrkernige Zellen mit prominenten Nukleolen), ANITSCHKOW Myozyten: Lange dünne Zelle mit elongiertem Kern.
Ät.: Wahrscheinlich Autoimmunreaktion durch Freisetzung von Antigen.
Klinik: Tage bis Wochen nach Infarkt Fieber, Brustschmerzen, abakterielle Myokarditis, Perikarditis und Pleuritis.
Mikro: Kaum Entzündung, kein Fibrin, wenige Immunzellen
Makro: Seröses Exsudat
Ät.: Urämie, Myokardinfarkt, akute rheumatische Carditis
Mikro: Fibrin, Entzündung
Makro: Fibrinstränge von Epi- zu Perikard, Epikard rauh und trüb, bread-and-butter-Phänomen
Wie fibrinöse Perikarditis mit Einblutung.
Mikro: Massenhaft Granulozyten, ggf. Bakterien
Makro: Eitrige, gelbliche Flüssigkeit im Perikard
Ät.: Transmuraler Herzinfarkt, perforiertes Herzwandaneurysma, Aortendissektion.
Makro: Das Perikard ist mit Blut gefüllt.
Klinik: Abruptes Herzversagen im obstruktiven Schock.
Zunahme der Herzmuskelmasse durch Zunahme der Zellgröße und der kontraktilen Elemente. Das kritische Herzgewicht beträgt abhängig von der Koronarreserve etwa 500 g.
Hypertrophie mit konstant bleibendem Herzinnenvolumen.
Makro: Das Myokard ist verdickt (normal 8-11mm 1cm unterhalb der Klappenebene), das Volumen vermindert, im Querschnitt ähnelt das Herz einem gotischen Bogen.
Kompl.: Erreichen des kritischen Herzgewichts -> Ischämie des Herzmuskels
Muskelhypertrophie mit Zunahme des Herzinnenvolumens.
Makro: Das Myokard ist verdickt, alle 4 Kammern sind dilatiert, das Herz ist globoid abgerundet und ähnelt einem römischen Bogen. Die Konsistenz ist weich und gummiartig.
Kompl.: Gefügedilatation -> Herzinsuffizienz
Hypertrophie des rechten Herzens
Makro: Die Wand des rechten Ventrikels ist verdickt (normal sind 2-4 mm Wandicke 1 cm unterhalb der Klappenebene).
Herzmuskelerkrankungen, die nicht durch mechanische Überlastung oder KHK verursacht sind. Ausgeschlossen werden müssen: KHK, mechanische Herzbelastung (z.B. Aorteklappenstenose, Mitralklappeninsuffizienz), arterielle Hypertonie und Myokarditis.
Formen der Kardiomyopathie:
Primärer Herztumor, selten
Makro: Große, solide, weiße Tumormasse.
Häufigster primärer Herztumor, benigne.
Makro: Runder, ballförmiger, an der Herzinnenwand des Atrium, seltener des Ventrikels oder an einer Klappe haftender Tumor. Dieser kann embolisieren oder den Blutfluß behindern.
Mikro: Leeres, sehr zellarmes, myxoides Stroma mit spindeligen Zellen.
Makro: Blasse, weißliche Knoten
Procedures of Tissue Preparation | Glossary | Resources
According to the Bible, the heart is the centre not only of spiritual activity, but of all the operations of human life. "Heart" and "soul" are often used interchangeably (Deut 6:5; 26:16; comp. Mt 22:37; Mk 12:30, 33), but this is not generally the case.
The heart is the "home of the personal life," and hence a man is designated, according to his heart, wise (1 Kg 3:12, etc.), pure (Ps 244; Mt 5:8, etc.), upright and righteous (Gen 20:5, 6; Ps 112; 78:72), pious and good (Lk 8:15), etc. In these and such passages the word "soul" could not be substituted for "heart."
The heart is also the seat of the conscience (Rom 2:15). It is naturally wicked (Gen 8:21), and hence it contaminates the whole life and character (Mt 12:34; 15:18; comp. Eccl 8:11; Ps 737). Hence the heart must be changed, regenerated (Ezek 36:26; 11:19; Ps 5110-14), before a man can willingly obey God.
The process of salvation begins in the heart by the believing reception of the testimony of God, while the rejection of that testimony hardens the heart (Ps 958; Prov 28:14; 2Chr 36:13). "Hardness of heart evidences itself by light views of sin; partial acknowledgment and confession of it; pride and conceit; ingratitude; unconcern about the word and ordinances of God; inattention to divine providences; stifling convictions of conscience; shunning reproof; presumption, and general ignorance of divine things."
what mentions this? (please help by turning references to this page into wiki links)
Sometimes hearts are used to show a kiss or an infatuated character in games where the graphics are not sophisticated enough to animate these actions. In some games, hearts are used in attack animations for female characters, such as Sexy Silvia's gun (which fires a glowing heart) or Amy Rose's Piko Piko Hammer (which explodes into hearts on impact.)
But typically, if you see a heart just laying around in any video game, pick it up. As a rule, hearts are always good.
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The heart is a muscle found in every animal that has a backbone. It is a very strong muscle that is about the size of a fist. It pumps blood through tubes called blood vessels. It has regular contractions, or when the heart squeezes the blood out into other parts of the body.
Cardiac means about the heart.
The human heart has four chambers or closed spaces. Some animals have only two or three chambers.
In humans, the four chambers are two atria and two ventricles. Atria is talking about two chambers; atrium is talking about one chamber. There is a right atrium and ventricle. These get blood that comes to the heart. They pump this blood to the lungs. In the lungs blood picks up oxygen and drops carbon dioxide. Blood from the lungs goes to the left atrium and ventricle. The left atrium and ventricle send the blood out to the body. The left ventricle works six times harder than the right ventricle because it carries oxygenated blood.
Blood is carried in blood vessels. These are arteries and veins. Blood going to the heart is carried in veins. Blood going away from the heart is carried in arteries. The main artery going out of the right ventricle is the pulmonary artery. (Pulmonary means about lungs.) The main artery going out of the left ventricle is the aorta.
The veins going into the right atrium are the superior vena cava and inferior vena cava. These bring blood from the body to the right heart. The veins going into the left atrium are the pulmonary veins. These bring blood from the lungs to the left heart.
When the blood goes from the atria to the ventricles it goes through heart valves. When blood goes out of the ventricles it goes through valves. The valves make sure that blood only goes one way in or out.
The four valves of the heart are:
The heart has three layers. The outer covering is the pericardium. This is a tough sack that surrounds the heart. The middle layer is the myocardium. This is the heart muscle. The inner layer is the endocardium. This is the thin smooth lining of the chambers of the heart.
A heart beat is when the heart muscle contracts. This means the heart pushes in and this makes the chambers smaller. This pushes blood out of the heart and into the blood vessels. After the heart contracts and pushes in, the muscle relaxes or stops pushing in. The chambers get bigger and blood coming back to the heart fills them.
When the heart muscle contracts (pushes in) it is called systole. When the heart muscle relaxes (stops pushing in), this is called diastole. Both atria do systole together. Both ventricles do systole together. But the atria do systole before the ventricles. Even though the atrial systole comes before ventricular systole, all four chambers do diastole at the same time. This is called cardiac diastole
The order is: atrial systole → ventricular systole → cardiac diastole. When this happens one time, it is called a cardiac cycle.
Systole (when the heart squeezes) happens because the muscle cells of the heart gets smaller in size. When they get smaller we also say they contract. Electricity going through the heart makes the cells contract. The electricity starts in the sino-atrial node (acronym SA Node) The SA Node is a group of cells in the right atria. These cells start an electrical impulse. This electrical impulse travels through the atria making them contract. This motion is called 'atrial systole'. Once electrical impulse goes through the atrio-ventricular node (acronym AV Node.) The AV Node makes the impulse slow down. Slowing down makes the electrical impulses get to the ventricles later. That is what makes the ventricular systole occur after atrial systole, and lets all the blood leave the atria before ventricle contracts (meaning squeeze).
After the electrical impulse goes through the AV Node, the electrical impulse will go through the conduction system of the ventricle. Conduction means heat or electricity traveling through something. This brings the electrical impulse to the ventricles. The first part of the conduction system is the bundle of His. His is named for the doctor (Wilhelm His, Jr) who discovered it. Bundle means strings or wires grouped together in parallel. Once the bundle (meaning a group of strings or wires going in parallel directions) goes through the ventricle muscle, it divides into two bundle branches, the left bundle branch and the right bundle branch. The left bundle branch travels to the left ventricle and the right bundle branch travels to the right ventricle. At the end of the bundle branches, the electrical impulse goes into the ventricular muscle through the Purkinje Fibers. This is what makes ventricle contraction take place and makes ventricular systole.
The order is: Sino-Atrial Node → Atria (systole) → Atrio-Ventricular Node → Bundle of His → Bundle branches → Purkinje Fibers → Ventricles (systole)
ECG is an acronym for ElectroCardioGram. It is also written EKG for ElectroKardioGram in German. The ECG shows what the electricity in the heart is doing. An EKG is done by putting electrodes on a person's skin. The electrodes see the electricity going through the heart. This is written on paper by a machine. This writing on the paper is the ECG.
Doctors learn about the person's heart by looking at the ECG. The ECG shows some diseases of the heart like heart attacks or problems with the rhythm of the heart (how the electricity goes through the heart's conduction system.)
The ECG shows atrial systole. This is called a P-wave. Then ventricular systole happens. This is called the QRS or QRS-complex. It is called a complex because there are three different waves in it. The Q-wave, R-wave, and S-wave. Then the ECG shows ventricular diastole. This is called the T-wave. Atrial diastole happens then too. But it is not seen separate from ventricular diastole.
The PR-Interval is the space between atrial systole (P) and ventricular systole (QRS). The QT-Interval is from when the QRS starts to when the T ends. The ST-segment is the space between the QRS and T.
[[File:|thumbnail|550px|ECG "Rhythm Strip" - Each QRS is one heart beat]]
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