Organs. Are separate body structures that perform specific functions. They are composed of two or more different tissues.
The heart is a hollow muscular organ, which receives blood from the venous trunks draining into it and pumps the blood into the arterial system. The cavity of the heart is subdivided into four chambers: two atria and two ventricles. The left atrium and the left ventricle comprise the left heart, also called the arterial heart, because of the type of blood it contains; the right atrium and right ventricle comprise the right or venous heart. The heart is located in the thoracic cavity between the lungs. This area is called the mediastinum. The base of the cone-shaped heart is uppermost, behind the sternum, and the great vessels enter or leave here. The apex (tip) of the heart points downward and is just above the diaphragm to the left of the midline. This is why we may think of the heart as being on the left side, because the strongest beat can be heard or felt here. The importance of the heart has been recognized for centuries. The fact that its rate of beating is affected by the emotions may be responsible for the very frequent references to the heart in song and poetry. However, the vital functions of the heart and its disorders are of more practical importance to us.
Figure 1.Human Heart.a) Anterior aspect. (b) Internal anatomy.
Location of the Heart and pericardial membranes
The human heart is located within the thoracic cavity, medially between the lungs in the space known as the mediastinum. Figure 2 shows the position of the heart within the thoracic cavity. Within the mediastinum, the heart is separated from the other mediastinal structures by a tough membrane known as the pericardium, or pericardial sac, and sits in its own space called the pericardial cavity. The dorsal surface of the heart lies near the bodies of the vertebrae, and its anterior surface sits deep to the sternum and costal cartilages. The great veins, the superior and inferior venae cavae, and the great arteries, the aorta and pulmonary trunk, are attached to the superior surface of the heart, called the base.
The base of the heart is located at the level of the third costal cartilage, as seen in Figure 2.The inferior tip of the heart, the apex, lies just to the left of the sternum between the junction of the fourth and fifth ribs near their articulation with the costal cartilages. The right side of the heart is deflected anteriorly, and the left side is deflected posteriorly. It is important to remember the position and orientation of the heart when placing a stethoscope on the chest of a patient and listening for heart sounds, and also when looking at images taken from a midsagittal perspective. The slight deviation of the apex to the left is reflected in a depression in the medial surface of the inferior lobe of the left lung, called the cardiac notch.
Figure 2. Position of the Heart in the Thorax
Figure 3.Layers of the wall of the heart and the pericardial membranes.
Shape and Size of the Heart
The shape of the heart is similar to a pinecone, rather broad at the superior surface and tapering to the apex (see Figure 2). A typical heart is approximately the size of an individual fist: 12 cm (5 in) in length, 8 cm (3.5 in) wide, and 6 cm (2.5 in) in thickness. Given the size difference between most members of the sexes, the weight of a female heart is approximately 250–300 grams (9 to 11 ounces), and the weight of a male heart is approximately 300–350 grams (11 to 12 ounces). The heart of a well-trained athlete, especially one specializing in aerobic sports, can be considerably larger than this. Cardiac muscle responds to exercise in a manner similar to that of skeletal muscle. That is, exercise results in the addition of protein myofilaments that increase the size of the individual cells without increasing their numbers, a concept called hypertrophy. Hearts of athletes can pump blood more effectively at lower rates than those of non-athletes. Enlarged hearts are not always a result of exercise; they can result from pathologies, such as hypertrophic cardiomyopathy. The cause of an abnormally enlarged heart muscle is unknown, but the condition is often undiagnosed and can cause sudden death in apparently otherwise healthy young people.
Chambers of the heart
The heart has four chambers. The two at the superior pole (base) of the heart are the right and left atria. They are thin walled receiving chambers for blood returning to the heart by way of the great veins. Most of the mass of each atrium is on the posterior side of the heart, so only a small portion is visible from the anterior aspect. Here, each atrium has a small earlike extension called an auricle6 that slightly increases its volume. The two inferior heart chambers are the right and left ventricles,are the pumps that eject blood into the arteries and keep it flowing around the body. The right ventricle constitutes most of the anterior aspect of the heart, while the left ventricle forms the apex and inferoposterior aspect.
The walls of the four chambers of the heart are made of cardiac muscle called the myocardium. The chambers are lined with endocardium, simple squamous epithelium that also covers the valves of the heart and continues into the vessels as their lining (endothelium). The important physical characteristic of the endocardium is not its thinness, but rather its smoothness. This very smooth tissue prevents abnormal blood clotting, because clotting would be initiated by contact of blood with a rough surface.
The right atrium
Is a thin-walled chamber that receives the blood retuning from the body tissues. This blood, which is low in oxygen, is carried in the veins, the blood vessels leading to the heart from the body tissues. From the right atrium, blood will flow through the right atrioventricular (AV) valve, or tricuspid valve, into the right ventricle.
The tricuspid valve is made of three flaps (or cusps) of endocardium reinforced with connective tissue. The general purpose of all valves in the circulatory system is to prevent backflow of blood. The specific purpose of the tricuspid valve is to prevent backflow of blood from the right ventricle to the right atrium when the right ventricle contracts. As the ventricle contracts, blood is forced behind the three valve flaps, forcing them upward and together to close the valve.
The inner surface of the right atrium is smooth except for a small frontal area and for the inner surface of the auricle where the pectinate muscles (musculi pectinati) form a series of small vertical columns. Superiorly the pectinate muscles are continuous with a crest (crista terminalis), to which the sulcus terminalis corresponds on the external surface of the atrium. This sulcus points to the site where the primary sinus venosus is connected with the atrium of the embryo. On the septum separating the right atrium from the left is an oval depression (fossa ovalis), which is bounded superiorly and anteriorly by a raised edge, annulus ovalis (limbus fossae ovalis). This depression is a remnant of the foramen ovale through which the atria communicate during the intrauterine period. The foramen ovale may persist throughout life (in one-third of all cases). On the posterior wall between the orifices of the superior and inferior venae cavae is a small ridge, intervenous tubercle (tuberculum intervenosus) to the back of the superior part of the fossae ovalis. This ridge is thought to direct the flow of blood in the embryo from the superior vena cava into the right atrioventricular orifice.
A fold of vena cava inferior (valvula venae cavae inferioris) stretches from the inferior margin of the orifice of the inferior vena cava to the limbus fossae ovalis. This fold is of vital importance for the embryo because it directs blood from the inferior vena cava through the foramen ovale into the left atrium. Below this valve, between the openings of the inferior vena cava and the right atrioventricular orifice, the sinus coronarius cordis, which collects blood from the veins of the heart, drains into the right atrium; moreover, small veins of the heart drain independently into the right atrium. Their small openings (foramina venarum minimarum) are scattered over the surface of the atrial walls. A small endocardial fold (valvula sinus coronarii) is found close to the opening of the venous sinus. In the inferoanterior section of the atrium, the wide right atrioventricular orifice (ostium atrioventriculare dextrum) leads into the cavity of the right ventricle.
The left atrium.
The left atrium (atrium sinistrum) adjoins posteriorly the descending aorta and the oesophagus. Two pulmonary veins drain into it from each side. The auricle of the left atrium (auricula sinistra) protrudes anteriorly, passing around the left side of the aorta and pulmonary trunk. The auricle contains pectinate muscles. In the inferoanterior section, an oval-shaped, left atrioventricular orifice (ostium atrioventriculare sinistrum) leads into the cavity of the left ventricle.
The right ventricle
The right ventricle pumps the venous blood received from the right atrium and sends it to the lungs. The wall of the right ventricle is smooth in the region of the conus arteriosus, but elsewhere there are inwardly projecting muscular trabeculae (trabeculae carneae). Between the longitudinal trabeculae lies a series of transverse ridges, as a result of which a network of trabeculae is produced.
Blood from the right ventricle enters the pulmonary trunk through an orifice, the ostium trunci pulmonalis, supplied with a valve, the valva trunci pulmonalis, which prevents the return of blood from the pulmonary trunk into the right ventricle during diastole. The valve is composed of three semilunar cusps called the semilunar valvulae. One of them is attached to the anterior third of the circumference of the pulmonary trunk (valvula semilunaris anterior) and the other two to the posterior section of the circumference (valvulae semilunares dextra and sinistra). A small nodule, the nodulus valvulae semilunaris, is found in the middle of the free inner border of each valve; on each side of this nodule there are thin marginal segments of the valve called the lunulae valvulae semilunares. The nodules make the valves close more tightly.
When the right ventricle contracts, the tricuspid valve closes and the blood is pumped to the lungs through the pulmonary artery (or trunk). At the junction of this large artery and the right ventricle is the pulmonary semilunar valve (or more simply, pulmonary valve). Its three flaps are forced open when the right ventricle contracts and pumps blood into the pulmonary artery. When the right ventricle relaxes, blood tends to come back, but this fills the valve flaps and closes the pulmonary valve to prevent backflow of blood into the right ventricle. Projecting into the lower part of the right ventricle are columns of myocardium called papillary muscles (see Fig. 4). Strands of fibrous connective tissue, the chordae tendineae, extend from the papillary muscles to the flaps of the tricuspid valve. When the right ventricle contracts, the papillary muscles also contract and pull on the chordae tendineae to prevent inversion of the tricuspid valve. If you have ever had your umbrella blown inside out by a strong wind, you can see what would happen if the flaps of the tricuspid valve were not anchored by the chordae tendineae and papillary muscles.
The left ventricle
The left ventricle als is a chamber of human heart which has the thickest walls of all, pumps, oxygenated blood to all parts of the body. This blood goes through the arteries, the vessels that take blood from the heart to the tissues. The walls of the left ventricle are thicker than those of the right ventricle, which enables the left ventricle to contract more forcefully. The left ventricle pumps blood to the body through the aorta, the largest artery of the body. At the junction of the aorta and the left ventricle is the aortic semilunar valve (or aortic valve) (see Fig. 4). This valve is opened by the force of contraction of the left ventricle, which also closes the mitral valve. The aortic valve closes when the left ventricle relaxes, to prevent backflow of blood from the aorta to the left ventricle. When the mitral (left AV) valve closes, it prevents backflow of blood to the left atrium; the flaps of the mitral valve are also anchored by chordae tendineae and papillary muscles.
Blood Flow through the Chambers
Until the sixteenth century, anatomists thought that blood flowed directly from the right ventricle to the left through invisible pores in the septum. This of course is not true. Blood in the right and left chambers of the heart is kept entirely separate. Figure 5 shows the pathway of the blood as it travels from the right atrium through the body and back to the starting point. The figure is numbered to correspond to the following description.
Figure.6The Pathway of Blood Flow Through the Heart.
- Approaching from above and below the heart, respectively. Blood in the right atrium flows through the right AV valve into the right ventricle
- When the right ventricle contracts, the AV valve closes and blood is forced through the pulmonary valve into the pulmonary trunk.This artery ascends from the front of the heart and branches into the right and left pulmonary arteries which lead to the respective lungs. In the lungs, this blood unloads its carbon dioxide and picks up a load of oxygen.
- The oxygen-enriched blood returns by way of several veins which converge to form four pulmonary veins by the time they reach the heart. These four empty into the left atrium.
- The left ventricle contracts at the same time as the right, and expels this blood through the aortic valve (11) into the ascending aorta.
- Blood in the aorta flows to every organ in the body (13), unloading some of its O2, picking up CO2 from the tissues, and returning to the heart via the venae cavae.
The coronary circulation is the most variable aspect of cardiac anatomy. The following description covers only the largest coronary blood vessels, and describes only the pattern seen in about 70% to 85% of persons. Immediately after the aorta leaves the left ventricle, it gives off a right and left coronary artery. The orifices of these two arteries lie deep in the pockets formed by the aortic valve cusps.
The left coronary artery (LCA) travels through the coronary sulcus under the left auricle and divides into two branches (fig. 7. The anterior interventricular branch travels down the anterior interventricular sulcus to the apex, rounds the bend, and travels a short distance up the posterior side of the heart. There it anastomoses with (joins) the posterior interventricular branch described shortly. Clinically, it is also called the left anterior descending (LAD) branch. This artery supplies blood to both ventricles and the anterior two-thirds of the interventricular septum.
Figure.7.The Coronary Blood Vessels (a) Anterior aspect. (b) Posterior aspect.
The right coronary artery (RCA) supplies the right atrium and sinoatrial node (pacemaker), continues along the coronary sulcus under the right auricle, and gives off two branches of its own:
- The right marginal branch runs toward the apex of the heart and supplies the lateral aspect of the right atrium and ventricle.
- The RCA continues around the right margin of the heart to the posterior side, sends a small branch to the atrioventricular node, then gives off a large posterior interventricular branch.
This branch travels down the corresponding sulcus and supplies the posterior walls of both ventricles as well as the posterior portion of the interventricular septum. It ends by anastomosing with the circumflex and anterior interventricular branches of the left coronary artery . The energy demand of the cardiac muscle is so critical that an interruption of the blood supply to any part of the myocardium can cause necrosis within minutes. A fatty deposit or blood clot in a coronary artery can cause a myocardial infarction (MI), the sudden death of a patch of tissue deprived of its blood flow).
Most organs receive more arterial blood when the ventricles contract than when they relax, but the opposite is true in the coronary arteries. There are three reasons for this. Contraction of the myocardium compresses the arteries and obstructs blood flow. During ventricular systole (contraction of the ventricles), the aortic valve is forced open and the valve cusps cover the openings to the coronary arteries, blocking blood from flowing into them.
During ventricular diastole (relaxation), blood in the aorta briefly surges back toward the heart. It fills the aortic valve cusps and some of it flows into the coronary arteries, like sand filling a shirt pocket and flowing out through a hole in the bottom. In the coronary blood vessels, therefore, diastolic blood flow is greater than systolic blood flow.
Membranes, Surface Features, and Walls
The membrane that directly surrounds the heart and defines the pericardial cavity is called the pericardium or pericardial sac. It also surrounds the “roots” of the major vessels, or the areas of closest proximity to the heart. The pericardium, which literally translates as “around the heart,” consists of two distinct sublayers: the sturdy outer fibrous pericardium and the inner serous pericardium. The fibrous pericardium is made of tough, dense connective tissue that protects the heart and maintains its position in the thorax. The more delicate serous pericardium consists of two layers: the parietal pericardium, which is fused to the fibrous pericardium, and an inner visceral pericardium, or epicardium, which is fused to the heart.The Cardiovascular System.
The Heart and is part of the heart wall. The pericardial cavity, filled with lubricating serous fluid, lies between the epicardium and the pericardium. In most organs within the body, visceral serous membranes such as the epicardium are microscopic. However, in the case of the heart, it is not a microscopic layer but rather a macroscopic layer, consisting of a simple squamous epithelium called a mesothelium, reinforced with loose, irregular, or areolar connective tissue that attaches to the pericardium. This mesothelium secretes the lubricating serous fluid that fills the pericardial cavity and reduces friction as the heart contracts.
Figure 8.The pericardial membrane and the layers of the heart.
Surface Features of the Heart
Inside the pericardium, the surface features of the heart are visible, including the four chambers. There is a superficial leaflike extension of the atria near the superior surface of the heart, one on each side, called an auricle a name that means “ear like” because its shape resembles the external ear of a human. Auricles are relatively thin-walled structures that can fill with blood and empty into the atria or upper chambers of the heart.
Major coronary blood vessels are located in these sulci. The deep coronary sulcus is located between the atria and ventricles. Located between the left and right ventricles are two additional sulci that are not as deep as the coronary sulcus. The anterior interventricular sulcus is visible on the anterior surface of the heart, whereas the posterior interventricular sulcus is visible on the posterior surface of the heart.
Structure of the heart walls
The walls of the heart are made up of three layers of unequal thickness. These layers are the inner layer, (the endocardium), a middle layer, (the myocardium), and an outer layer, the (epicardium), which is the visceral membrane of the pericardium. The thickness of the cardiac walls consists mainly of the middle layer, the myocardium, made up of muscle tissue. The outer layer, the epicardium, is the visceral lining of the serous pericardium. The inner layer, the endocardium, lines the heart cavities. Although the myocardium, or the muscle tissue of the heart, is cardiac striated, it differs from the skeletal muscles in that it consists not of symplasts, but of a network of contiguous, mononuclear cells joined to form fibres.
Two layers are distinguished in the heart musculature: the muscular layers of the atrium and the muscular layers of the ventricles. The fibres of both arise from two fibrous rings (anuli fibrosi) one of which surrounds the right atrioventricular orifice and the other, the left atrioventricular orifice. The fibres of the atrium contract separately from the ventricles. A superficial and a deep muscular layer are distinguished in the atria: the superficial layer consists of circular or transverse fibres, whereas the deep layer is made up of longitudinal fibres arising from the fibrous rings and encircling the atrium like a loop. The large venous trunks draining into the atria are surrounded by circular fibres like sphincters. The fibres of the superficial layer encircle both atria; the deep fibres are separate in each atrium.
The musculature of the ventricles is even more complex. Three layers can be distinguished in it. A thin superficial layer is composed of longitudinal fibres which arise from the right fibrous ring and descend obliquely, passing also onto the left ventricle; on the heart apex, they form a whorled mass (vortex cordis), making loops in the depths of the muscle and forming the longitudinal inner layer; the upper ends of the fibres of this layer are attached to the fibrous rings. The fibres of the middle layer, between the longitudinal outer and inner layers, are more or less circular. In contrast to the fibres of, the superficial layer, however, they do not pass from one ventricle to the other but are independent components of each ventricle.
The epicardiumIs a serious membrane on the heart surface. It consists mainly of a simple squamous epithelium overlying a thin layer of areolar tissue. In some places, it also includes a thick layer of adipose tissue, whereas in other areas it is fat-free and translucent.The largest branches of the coronary blood vessels travel through the epicardium.A similar layer, the endocardium, lines the interior of the heart chambers. It is a simple squamous endothelium overlying a thin areolar tissue layer; it has no adipose tissue. The endocardium covers the valve surfaces and is continuous with the endothelium of the blood vessels.The epicardium covers the outer surface of the myocardium and is an ordinary serous membrane lined by the mesothelium. The underlying structures can be seen through the transparent epicardium: the middle layer of the heart (myocardium), vessels, nerves, and subepicardial fatty tissue. The latter lies along the coronary and interventricular grooves of the vessels.
The endocardium is a very thin smooth layer of cells that resembles squamous epithelium. This membrane lines the interior of the heart. The valves of the heart are formed by reinforced folds of this material. The endocardium forms the lining of the inner surface of the heart cavities. It is made up, in turn, of a layer of connective tissue rich in elastic fibres and smooth muscle cells, a layer of connective tissue over the first layer with an admixture of elastic fibres, and an inner endothelial layer, the presence of which distinguishes the endocardium from the epicardium. In origin, the endocardium corresponds to the vascular wall, while its three layers correspond to the three vascular coats. All the heart valves are folds of the endocardium. The myocardium, the muscle of the heart, is the thickest layer.
The heart also has a meshwork of collagenous and elastic fibers that make up the fibrous skeleton. This tissue is especially concentrated in the walls (septa) between the heart chambers, in fibrous rings (annuli fibrosi) around the openings of the heart valves, and in sheets of tissue that interconnect these rings. The fibrous skeleton has multiple functions:
- It provides structural support for the heart, especially around the valves and the openings of the great vessels; it holds the valve orifices open and prevents them from being excessively stretched when blood surges through them.
- It anchors the myocytes and gives them something to pull against.
- As a nonconductor of electricity, it serves as electrical insulation between the atria and the ventricles, so the atria cannot stimulate the ventricles directly. This insulation is important to the timing and coordination of electrical and contractile activity.
- Some authorities think (while others disagree) that elastic recoil of the fibrous skeleton may aid in refilling the heart with blood after each beat, like a hollow rubber ball that expands when you relax your grip.
Internal Structure of the Heart
Recall that the heart’s contraction cycle follows a dual pattern of circulation the pulmonary and systemic circuits because of the pairs of chambers that pump blood into the circulation. In order to develop a more precise understanding of cardiac function, it is first necessary to explore the internal anatomical structures in more detail.
Septa of the Heart.
The word septum is derived from the Latin for “something that encloses;” in this case, a septum (plural = septa) refers to a wall or partition that divides the heart into chambers. The septa are physical extensions of the myocardium lined with endocardium. Located between the two atria is the interatrial septum. Normally in an adult heart, the interatrial septum bears an oval-shaped depression known as the fossa ovalis, a remnant of an opening in the fetal heart known as the foramen ovale. The foramen ovale allowed blood in the fetal heart to pass directly from the right atrium to the left atrium, allowing some blood to bypass the pulmonary circuit. Within seconds after birth, a flap of tissue known as the septum primum that previously acted as a valve closes the foramen ovale and establishes the typical cardiac circulation pattern.
The septum between the atria and ventricles is known as the atrioventricular septum. It is marked by the presence of four openings that allow blood to move from the atria into the ventricles and from the ventricles into the pulmonary trunk and aorta. Located in each of these openings between the atria and ventricles is a valve, a specialized structure that ensures one-way flow of blood.
The valves between the atria and ventricles are known generically as atrioventricular valves. The valves at the openings that lead to the pulmonary trunk and aorta are known generically as semilunar valves. The interatrial septum is not visible, since its location is covered by the aorta and pulmonary trunk. Since these openings and valves structurally weaken the atrioventricular septum, the remaining tissue is heavily reinforced with dense connective tissue called the cardiac skeleton, or skeleton of the heart. It includes four rings that surround the openings between the atria and ventricles, and the openings to the pulmonary trunk and aorta, and serve as the point of attachment for the heart valves. The cardiac skeleton also provides an important boundary in the heart electrical conduction system. Between the two ventricles is a second septum known as the interventricular septum. Unlike the interatrial septum, the interventricular septum is normally intact after its formation during fetal development. It is substantially thicker than the interatrial septum, since the ventricles generate far greater pressure when they contract.
The heart Valves.
The heart consists four valves which are in two pairs: Atrioventricular (AV) valves between atria and ventricles and semilunar valves between ventricles and main arteries. The heart valves are made of tough, rubbery flaps, called cusps, which grow out of the heart wall. Joined to the free ends of the AV valves are a number of cords called chordae tendineae (heart strings) attaching them to muscles in the wall of the ventricle. The heart strings keep the AV flaps pointing in the direction of the blood flow, stopping them being turned “inside out” and forced through into the atria. The semilunar valves do not have heart strings. Blood flowing the wrong way makes the cusps balloon out so that their edges seal tight. Since the ventricles are the pumping chambers, the valves, which are all one way, are located at the entrance and the exit of each ventricle. The entrances valves are the atrioventricular valves, while the exit valves are the semilunar valves. Semilunar means “resembling a half moon.
As the heart valves slap shut to prevent the backflow of blood, they make a “lub-dub” sound. The “lub” is the AV valves closing, while the “dub” is the sound of the semilunar valves shutting.
The tricuspid valve consists of three cusps, while the bicuspid, or mitral, valve has only two cusps. They both stop blood flowing back from ventricles to atria.Atrioventricular (AV) valves AV valves prevent the backflow of blood from the ventricles to the atria when the heart contracts through the following merchanism.
- Blood fills the atria. The AV valves are closed.
- Pressure in the atria rises, forcing the valves open. The ventricles begin to fill with blood.
- As the ventricles become full, the AV valves close. This prevents blood from returning to the atria.
Classification of Atrioventricular valves.
The right atrioventricular valve also is known as the tricuspid valve, since it has three cusps, or flaps, that open and closes. When this valve is open, blood flows freely from the right atrium into the right ventricle. However, when the right ventricle begins to contract, the valve closes so that blood cannot return to the right atrium; this ensures forward flow into the pulmonary artery.
The left atrioventricular valve is the bicuspid valve, but it is usually referred to as the mirtal valve. It has two rather heavy cusps that permit blood to flow freely from the left atrium into the left ventricle. However, the cusps close when the left ventricle begins to contract; this prevents blood from returning to the left atrium and ensures the forward flow of blood into the aorta. Both the tricuspid and mitral valves are attached by means of thin fibrous threads to the wall of the ventricles. The function of these threads, called the chordae tendineae is to keep the valve flaps from flipping up into the atria when the ventricles contract and thus causing a backflow of blood.
The aortic semilunar valve and pulmonary semilunar valve are located at the base of the two large arteries leaving the heart (the aorta and pulmonary artery). Each is crescent-shaped and consists of three cusps.
The semilunar valves prevent the backflow of blood into the ventricles through the following mechanisms
- The ventricles contract until pressure exceeds that of blood in the aorta and pulmonary artery.
- The semilunar valves are forced open and blood flows out of the heart.
- The ventricles relax and blood begins to flow backward toward the heart. The cusps of the semilunar valves are filled with blood and they close. Blood is prevented from flowing back into the ventricles.
Classification of semilunar valves.
The pulmonic (semilunar) valve is located between the right ventricle and the pulmonary artery that leads to the lungs. As soon as the right ventricle has finished emptying itself, the valve closes in order to prevent blood on its way to the lungs from returning to the ventricle.
The aortic (semilunar) valve is located between the left ventricle and the aorta. Following contraction of the left ventricle, the aortic valve closes to prevent the flow of blood back from the aorta to the ventricle. Blood Supply to the Myocardium Although blood flows through the heart chambers, only the endocardium comes into contact with it. Therefore, the myocardium must have its own blood vessels to provide oxygen and nourishment and to remove waste products. The arteries that supply blood to the muscle of the heart are called the right and left coronary arteries. These arteries, which are the first branches of the aorta, arise just above the aortic semilunar valve. They receive blood when the heart relaxes. After passing through capillaries in the myocardium, blood drains into the cardiac veins and finally into the coronary (venous) sinus for return to the right atrium.
Physiology of the Heart
To listen to the heart beating, doctors and nurses position a stethoscope between the fifth and sixth ribs on a line leading down from the middle of the left collar bone. This area is directly over the apex of the heart, which moves forward when the heart ventricles contract and strikes the wall of the thorax. This can be felt from the outside of the chest as a heartbeat.
Heart’s pumping power
The middle layer of the heart’s wall is a thick layer of heart, or cardiac, muscle, known as myocardium (“myo” means muscle). The myocardium consists of three spiral layers of cardiac muscle attached to a framework of dense fibrous tissue that forms the “skeleton” of the heart. The spiral is the best arrangement for squeezing blood out of the heart’s chambers. The thickest heart muscle is in the wall of the left ventricle, which pumps blood all the way to the fingers and toes and back again. The right ventricle only has to pump blood to the lungs, so its walls are less than half as thick as those of the left ventricle. The atrial walls have much less muscle than the ventricle walls and so are quite thin. The left atrial wall is, however, thicker than the right atrial wall. Rings of cardiac muscle around the tricuspid and mitral inlet valves lock them tightly shut when the ventricles pump blood to the body and lungs. Cardiac muscle contains bundles of actin and myosin filaments and contracts in the same way as other body muscles. But it differs from other muscles in the way that nerve signals travel through the fibers and stimulate the muscle to contract.
Heart muscle structure
Cardiac muscle is different from the other two types of muscle in the body. It has stripes, like skeletal muscle, but works as a coordinated unit, rather than as a group of separate units, as skeletal muscle does. Cardiac muscle cells act together because they are connected by intercalated discs. These electrical connectors allow nerve impulses to travel through the heart without stopping.
Heart muscle responds to the autonomic or involuntary nervous system, as well as to its own internally generated electrical commands. It is not under conscious control, and works automatically, like the smooth muscle that lines the stomach and other internal organs.
- The fibrous skeleton of the heart, together with the valves inside the heart, make up about half of the heart’s weight.
- The wall of the left ventricle is up to half an inch (1.3 cm) thick in some places.
The Work of the Heart
A complete heartbeat is called the cardiac cycle. One heartbeat means the contraction (also called systole) and relaxation (diastole) of the atria, followed by the contraction and relaxation of the ventricles. Each cardiac cycle takes about 0.8 seconds to complete if the heart beats at an average of 72 beats per minute. In a normal heartbeat, the two atria contract simultaneously while the two ventricles relax. When the two ventricles contract, both atria relax. During a typical heartbeat, the atria contract for about 10 percent of the time and the ventricles for about 40 percent. The direction of blood flow through the the heart is controlled by the atrioventricular (AV) and semilunar valves.
Although the right and left side of the heart are separated from each other, they work together. The blood is squeezed through the chambers by a contraction of heart muscle beginning in the thin-walled upper chambers, the atria, followed by a contraction of the thick muscle of the lower chambers, the ventricles. This active phase is called systole, and in each case it is followed by a resting period known as diastole. The contraction of the walls of the atria is completed at the time the contraction of the ventricles begins. Thus, the resting phase (diastole) begins in the atria at the same time as the contraction (systole) begins in the ventricles.
After the ventricles have emptied, both chambers are relaxed for a short period of time as they fill with blood. Then another beat begins with contraction of the ventricles. This sequence of heart relaxation and contraction is called the cardiac cycle. Each cycle takes an average of 0.8 seconds.
Cardiac muscle tissue has several unique properties.
- Interconnection of the muscle fibers. The fibers are interwoven so the stimulation that causes the contraction of one fiber results in the contraction of the whole group. This plays an important role in the process of conduction and the working of the heart muscle.
- Another property of heart muscle is its ability to adjust contraction strength to the amount of blood received. When the heart chamber is filled and the wall stretched (within limits), the contraction is strong. As less blood enters the heart, the contraction becomes weaker. As more blood enters the heart, as occurs during exercise, the muscle contracts, with greater strength so push the larger volume of blood out into the blood vessels.
The volume of blood pumped by each ventricle in 1 minute is termed the cardiac output. It is determined by the volume of blood ejected from the ventricle with each beat−the stroke volume−and the number of beats of the heart per minute−the heart rate. The cardiac output averages 5 litres/minute for an adult at rest.
Heart disease is the leading cause of death in the United States (about 30% of deaths per annum, averaged across all age groups). The most common form of heart disease is coronary atherosclerosis, often leading to myocardial infarction. However, there are a multitude of other heart diseases. The principal categories of heart disease are congenital defects in cardiac anatomy, myocardial hypertrophy or degeneration, inflammation of the pericardium and heart wall, valvular defects, and cardiac tumors.
THE CARDIAC CONDUCTION SYSTEM AND CARDIAC MUSCLE
The most obvious physiological fact about the heart is its rhythmicity. It contracts at regular intervals, typically about 75 beats per minute (bpm) in a resting adult. Among invertebrates such as clams, crabs, and insects, each heartbeat is triggered by a pace maker in the nervous system. The vertebrate heartbeat, however, is said to be myogenic because the signal originates within the heart itself. Indeed, we can remove the heart from the body, keep it in aerated saline, and it will beat for hours. Cut the heart into little pieces, and each piece continues its own rhythmic pulsations. Thus it is obviously not dependent on the nervous system for its rhythm. The heart has its own pacemaker and electrical conduction system, and it is to this system that we now turn our attention.Cardiac muscle undergoes aerobic respiration patterns, primarily metabolizing lipids and carbohydrates. Myoglobin, lipids, and glycogen are all stored within the cytoplasm. Cardiac muscle cells undergo twitch-type contractions with long refractory periods followed by brief relaxation periods. The relaxation is essential so the heart can fill with blood for the next cycle. The refractory period is very long to prevent the possibility of tetany, a condition in which muscle remains involuntarily contracted. In the heart, tetany is not compatible with life, since it would prevent the heart from pumping blood.
Recall that cardiac muscle shares a few characteristics with both skeletal muscle and smooth muscle, but it has some unique properties of its own. Not the least of these exceptional properties is its ability to initiate an electrical potential at a fixed rate that spreads rapidly from cell to cell to trigger the contractile mechanism. This property is known as autorhythmicity. Neither smooth nor skeletal muscle can do this. Even though cardiac muscle has autorhythmicity, heart rate is modulated by the endocrine and nervous systems. There are two major types of cardiac muscle cells: myocardial contractile cells and myocardial conducting cells. The myocardial contractile cells constitute the bulk (99 percent) of the cells in the atria and ventricles. Contractile cells conduct impulses and are responsible for contractions that pump blood through the body. The myocardial conducting cells (1 percent of the cells) form the conduction system of the heart. Except for Purkinje cells, they are generally much smaller than the contractile cells and have few of the myofibrils or filaments needed for contraction. Their function is similar in many respects to neurons, although they are specialized muscle cells. Myocardial conduction cells initiate and propagate the action potential (the electrical impulse) that travels throughout the heart and triggers the contractions that propel the blood.
Structure of Cardiac Muscle Compared to the giant cylinders of skeletal muscle, cardiac muscle cells, or cardiomyocytes, are considerably shorter with much smaller diameters. Cardiac muscle also demonstrates striations, the alternating pattern of dark A bands and light I bands attributed to the precise arrangement of the myofilaments and fibrils that are organized in sarcomeres along the length of the cell.These contractile elements are virtually identical to skeletal muscle. T (transverse) tubules penetrate from the surface plasma membrane, the sarcolemma, to the interior of the cell, allowing the electrical impulse to reach the interior. The T tubules are only found at the Z discs, whereas in skeletal muscle, they are found at the junction of the A and I bands. Therefore, there are one-half as many T tubules in cardiac muscle as in skeletal muscle. In addition, the sarcoplasmic reticulum stores few calcium ions, so most of the calcium ions must come from outside the cells. The result is a slower onset of contraction. Mitochondria are plentiful, providing energy for the contractions of the heart. Typically, cardiomyocytes have a single, central nucleus, but two or more nuclei may be found in some cells. Cardiac muscle cells branch freely. A junction between two adjoining cells is marked by a critical structure called an intercalated disc, which helps support the synchronized contraction of the muscle. The sarcolemmas from adjacent cells bind together at the intercalated discs. They consist of desmosomes, specialized linking proteoglycans, tight junctions, and large numbers of gap junctions that allow the passage of ions between the cells and help to synchronize the contraction. Intercellular connective tissue also helps to bind the cells together. The importance of strongly binding these cells together is necessitated by the forces exerted by contraction.
The Conduction System
Cardiac myocytes (muscle cells) are said to be autorhythmic15 because they depolarize spontaneously at regular time intervals. Some of them lose the ability to contract and become specialized, instead, for generating action potentials. These cells constitute the cardiac conduction system, which controls the route and timing of electrical conduction to ensure that the four chambers are coordinated with each other.
Electrical signals arise and travel through the cardiac conduction system in the following order (fig.14):
- The sinoatrial (SA) node, a patch of modified myocytes in the right atrium, just under the epicardium near the superior vena cava. This is the pacemaker that initiates each heartbeat and determines the heart rate. Signals from the SA node spread throughout the atria, as shown by the yellow arrows in figure 14.
- The atrioventricular (AV) node, located near the right AV valve at the lower end of the interatrial septum. This node acts as an electrical gateway to the ventricles; the fibrous skeleton acts as an insulator to prevent currents from getting to the ventricles by any other route.
- The atrioventricular (AV) bundle (bundle of His16), a pathway by which signals leave the AV node. The AV bundle soon forks into right and left bundle branches, which enter the interventricular septum and descend toward the apex.
- Fibers, nervelike processes that arise from the lower end of the bundle branches and turn upward to spread throughout the ventricular myocardium. Purkinje fibers distribute the electrical excitation to the myocytes of the ventricles. They form a more elaborate network in the left ventricle than in the right.
Although the SA node is the normal pacemaker of the heart, other autorhythmic sites in the heart can fire and stimulate cardiac contraction if the SA node fails to fire first. These other sites usually fire at slower rates than the SA node and therefore do not assume a pacemaker role unless the SA node is diseased.When another site does assume such a role, it is called an ectopic focus. The AV node is the most common ectopic focus, but other areas of myocardium can also take on this role. Ectopic foci usually fire too slowly to sustain life.
Cardiac output is the amount of blood pumped by a ventricle in 1 minute. A certain level of cardiac output is needed at all times to transport oxygen to tissues and to remove waste products. During exercise, cardiac output must increase to meet the body’s need for more oxygen. We will return to exercise after first considering resting cardiac output. To calculate cardiac output, we must know the pulse rate and how much blood is pumped per beat. Stroke volume is the term for the amount of blood pumped by a ventricle per beat; an average resting stroke volume is 60 to 80 mL per beat. A simple formula then enables us to determine cardiac output:
Notice that the athlete’s resting stroke volume is significantly higher than the average. The athlete’s more efficient heart pumps more blood with each beat and so can maintain a normal resting cardiac output with fewer beats. Now let us see how the heart responds to exercise. Heart rate (pulse) increases during exercise, and so does stroke volume. The increase in stroke volume is the result of Starling’s law of the heart, which states that the more the cardiac muscle fibers are stretched, the more forcefully they contract. During exercise, more blood returns to the heart; this is called venous return. Increased venous return stretches the myocardium of the ventricles, which contract more forcefully and pump more blood, thereby increasing stroke volume. Therefore, during exercise, our formula might be the following:
Cardiac output = stroke volume x pulse
Cardiac output = 100 mL X 100 bpm
Cardiac output = 10,000 mL (10 liters)
This exercise cardiac output is twice the resting cardiac output we first calculated, which should not be considered unusual. The cardiac output of a healthy young person may increase up to four times the resting level during strenuous exercise. This difference is the cardiac reserve, the extra volume the heart can pump when necessary. If resting cardiac output is 5 liters and exercise cardiac output is 20 liters, the cardiac reserve is 15 liters. The marathon runner’s cardiac output may increase six times or more compared to the resting level, and cardiac reserve is even greater than for the average young person; this is the result of the marathoner’s extremely efficient heart. Because of Starling’s law, it is almost impossible to overwork a healthy heart. No matter how much the volume of venous return increases, the ventricles simply pump more forcefully and increase the stroke volume and cardiac output. Also related to cardiac output, and another measure of the health of the heart, is the ejection fraction. This is the percent of the blood in a ventricle that is pumped during systole. A ventricle does not empty completely when it contracts, but should pump out 60% to 70% of the blood within it. A lower percentage would indicate that the ventricle is weakening.
The period of time that begins with contraction of the atria and ends with ventricular relaxation is known as the cardiac cycle (Figure 15). The period of contraction that the heart undergoes while it pumps blood into circulation is called systole. The period of relaxation that occurs as the chambers fill with blood is called diastole.
The electrical event, the wave of depolarization, is the trigger for muscular contraction. The wave of depolarization begins in the right atrium, and the impulse spreads across the superior portions of both atria and then down through the contractile cells. The contractile cells then begin contraction from the superior to the inferior portions of the atria, efficiently pumping blood into the ventricles.
Phases of the Cardiac Cycle
- At the beginning of the cardiac cycle, both the atria and ventricles are relaxed (diastole).
- Blood is flowing into the right atrium from the superior and inferior venae cavae and the coronary sinus.
- Blood flows into the left atrium from the four pulmonary veins.
- The two atrioventricular valves, the tricuspid and mitral valves, are both open, so blood flows unimpeded from the atria and into the ventricles. Approximately 70–80 percent of ventricular filling occurs by this method.
- The two semilunar valves, the pulmonary and aortic valves, are closed, preventing backflow of blood into the right and left ventricles from the pulmonary trunk on the right and the aorta on the left.
Atrial Systole and Diastole
Contraction of the atria follows depolarization, represented by the P wave of the ECG. As the atrial muscles contract from the superior portion of the atria toward the atrioventricular septum, pressure rises within the atria and blood is pumped into the ventricles through the open atrioventricular (tricuspid, and mitral or bicuspid) valves. At the start of atrial systole, the ventricles are normally filled with approximately 70–80 percent of their capacity due to inflow during diastole. Atrial contraction, also referred to as the “atrial kick,” contributes the remaining 20–30 percent of filling (see Figure 15).
Atrial systole lasts approximately 100 ms and ends prior to ventricular systole, as the atrial muscle returns to diastole. Ventricular Systole Ventricular systole (see Figure 15) follows the depolarization of the ventricles and is represented by the QRS complex in the ECG. It may be conveniently divided into two phases, lasting a total of 270 ms. At the end of atrial systole and just prior to atrial contraction, the ventricles contain approximately 130 mL blood in a resting adult in a standing position. This volume is known as the end diastolic volume (EDV) or preload. Initially, as the muscles in the ventricle contract, the pressure of the blood within the chamber rises, but it is not yet high enough to open the semilunar (pulmonary and aortic) valves and be ejected from the heart. However, blood pressure quickly rises above that of the atria that are now relaxed and in diastole. This increase in pressure causes blood to flow back toward the atria, closing the tricuspid and mitral valves.
Since blood is not being ejected from the ventricles at this early stage, the volume of blood within the chamber remains constant. Consequently, this initial phase of ventricular systole is known as isovolumic contraction, also called isovolumetric contraction (see Figure 15). In the second phase of ventricular systole, the ventricular ejection phase, the contraction of the ventricular muscle has raised the pressure within the ventricle to the point that it is greater than the pressures in the pulmonary trunk and the aorta. Blood is pumped from the heart, pushing open the pulmonary and aortic semilunar valves. Pressure generated by the left ventricle will be appreciably greater than the pressure generated by the right ventricle, since the existing pressure in the aorta will be so much higher. Nevertheless, both ventricles pump the same amount of blood.
This quantity is referred to as stroke volume. Stroke volume will normally be in the range of 70–80 mL. Since ventricular systole began with an EDV of approximately 130 mL of blood, this means that there is still 50–60 mL of blood remaining in the ventricle following contraction. This volume of blood is known as the end systolic volume (ESV). Ventricular Diastole Ventricular relaxation, or diastole, follows repolarization of the ventricles and is represented by the T wave of the ECG. It too is divided into two distinct phases and lasts approximately 430 ms. During the early phase of ventricular diastole, as the ventricular muscle relaxes, pressure on the remaining blood within the ventricle begins to fall. When pressure within the ventricles drops below pressure in both the pulmonary trunk and aorta, blood flows back toward the heart, producing the dicrotic notch (small dip) seen in blood pressure tracings. The semilunar valves close to prevent backflow into the heart. Since the atrioventricular valves remain closed at this point, there is no change in the volume of blood in the ventricle, so the early phase of ventricular diastole is called the isovolumic ventricular relaxation phase, also called isovolumetric ventricular relaxation phase (see Figure 15). In the second phase of ventricular diastole, called late ventricular diastole, as the ventricular muscle relaxes, pressure on the blood within the ventricles drops even further. Eventually, it drops below the pressure in the atria. When this occurs, blood flows from the atria into the ventricles, pushing open the tricuspid and mitral valves. As pressure drops within the ventricles, blood flows from the major veins into the relaxed atria and from there into the ventricles. Both chambers are in diastole, the atrioventricular valves are open, and the semilunar valves remain closed (see Figure 15). The cardiac cycle is complete.
Atrioventricular (AV) Node The atrioventricular (AV) node is a second clump of specialized myocardial conductive cells, located in the inferior portion of the right atrium within the atrioventricular septum. The septum prevents the impulse from spreading directly to the ventricles without passing through the AV node. There is a critical pause before the AV node depolarizes and transmits the impulse to the atrioventricular bundle. This delay in transmission is partially attributable to the small diameter of the cells of the node, which slow the impulse. Also, conduction between nodal cells is less efficient than between conducting cells. These factors mean that it takes the impulse approximately 100 ms to pass through the node. This pause is critical to heart function, as it allows the atrial cardiomyocytes to complete their contraction that pumps blood into the ventricles before the impulse is transmitted to the cells of the ventricle itself. With extreme stimulation by the SA node, the AV node can transmit impulses maximally at 220 per minute. This establishes the typical maximum heart rate in a healthy young individual. Damaged hearts or those stimulated by drugs can contract at higher rates, but at these rates, the heart can no longer effectively pump blood.
A heart block refers to an interruption in the normal conduction pathway. The nomenclature for these is very straightforward. SA nodal blocks occur within the SA node. AV nodal blocks occur within the AV node. Infra-Hisian blocks involve the bundle of His. Bundle branch blocks occur within either the left or right atrioventricular bundle branches.
Pressures and Flow.
Fluids, whether gases or liquids, are materials that flow according to pressure gradients that is, they move from regions that are higher in pressure to regions that are lower in pressure. Accordingly, when the heart chambers are relaxed (diastole), blood will flow into the atria from the veins, which are higher in pressure. As blood flows into the atria, the pressure will rise, so the blood will initially move passively from the atria into the ventricles. When the action potential triggers the muscles in the atria to contract (atrial systole), the pressure within the atria rises further, pumping blood into the ventricles. During ventricular systole, pressure rises in the ventricles, pumping blood into the pulmonary trunk from the right ventricle and into the aorta from the left ventricle. Again, as you consider this flow and relate it to the conduction pathway, the elegance of the system should become apparent.
One of the simplest, yet effective, diagnostic techniques applied to assess the state of a patient’s heart is auscultation using a stethoscope. In a normal, healthy heart, there are only two audible heart sounds: S1 and S2. S1 is the sound created by the closing of the atrioventricular valves during ventricular contraction and is normally described as a “lub,” or first heart sound. The second heart sound, S2, is the sound of the closing of the semilunar valves during ventricular diastole and is described as a “dub” . In both cases, as the valves close, the openings within the atrioventricular septum guarded by the valves will become reduced, and blood flow through the opening will become more turbulent until the valves are fully closed. There is a third heart sound, S3, but it is rarely heard in healthy individuals. It may be the sound of blood flowing into the atria, or blood sloshing back and forth in the ventricle, or even tensing of the chordae tendineae. S3 may be heard in youth, some athletes, and pregnant women. If the sound is heard later in life, it may indicate congestive heart failure, warranting further tests. Some cardiologists refer to the collective S1, S2, and S3 sounds as the “Kentucky gallop,” because they mimic those produced by a galloping horse. The fourth heart sound, S4, results from the contraction of the atria pushing blood into a stiff or hypertrophic ventricle, indicating failure of the left ventricle. S4 occurs prior to S1 and the collective sounds S4, S1, and S2 are referred to by some cardiologists as the “Tennessee gallop,” because of their similarity to the sound produced by a galloping horse with a different gait.
Correlation Between Heart Rates and Cardiac Output.
Initially, physiological conditions that cause HR to increase also trigger an increase in SV. During exercise, the rate of blood returning to the heart increases. However as the HR rises, there is less time spent in diastole and consequently less time for the ventricles to fill with blood. Even though there is less filling time, SV will initially remain high. However, as HR continues to increase, SV gradually decreases due to decreased filling time. CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV. Consider this phenomenon in a healthy young individual. Initially, as HR increases from resting to approximately 120 bpm, CO will rise. As HR increases from 120 to 160 bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV. As HR continues to rise above 160 bpm, CO actually decreases as SV falls faster than HR increases. So although aerobic exercises are critical to maintain the health of the heart, individuals are cautioned to monitor their HR to ensure they stay within the target heart rate range of between 120 and 160 bpm, so CO is maintained. The target HR is loosely defined as the range in which both the heart and lungs receive the maximum benefit from the aerobic workout and is dependent upon age.
Cardiovascular Centers Nervous control over HR is centralized within the two paired cardiovascular centers of the medulla oblongata (Figure 16). The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve, cranial nerve X. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone.
This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately 100 bpm.Both sympathetic and parasympathetic stimulations flow through a paired complex network of nerve fibers known as the cardiac plexus near the base of the heart. The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes, plus additional fibers to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers.
Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (NE) at the neuromuscular junction of the cardiac nerves. NE shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increase in HR. It opens chemical- or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions. NE binds to the beta-1 receptor. Some cardiac medications (for example, beta blockers) work by blocking these receptors, thereby slowing HR and are one possible treatment for hypertension. Overprescription of these drugs may lead to bradycardia and even stoppage of the heart.
Input to the Cardiovascular Center
The cardiovascular center receives input from a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system. Collectively, these inputs normally enable the cardiovascular centers to regulate heart function precisely, a process known as cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons.
Prenatal Development of the Heart
The heart is one of the earliest organs to form and begin functioning in the embryo. The first traces of the heart appear in week 3; by 21 to 23 days (usually before the mother is aware that she is pregnant) the heart is already beating; by day 24, it circulates blood throughout the embryo. The critical early development of the heart is reflected by the prominent heart bulge that appears on the anterior surface of the embryo. In week 3, a region of mesoderm at the far anterior end of the embryo condenses into a pair of longitudinal cellular cords. By day 19, these become hollow, parallel endocardial heart tubes (fig. 17a). As the embryo grows and the head region folds, these tubes are pushed closer together, the tissues dividing them break down, and they fuse into a single heart tube (fig. 17b).
The heart forms from an embryonic tissue called mesoderm around 18 to 19 days after fertilization. Mesoderm is one of the three primary germ layers that differentiates early in development that collectively gives rise to all subsequent tissues and organs. The heart begins to develop near the head of the embryo in a region known as the cardiogenic area. Following chemical signals called factors from the underlying endoderm (another of the three primary germ layers), the cardiogenic area begins to form two strands called the cardiogenic cords. As the cardiogenic cords develop, a lumen rapidly develops within them. At this point, they are referred to as endocardial tubes. The two tubes migrate together and fuse to form a single primitive heart tube. The primitive heart tube quickly forms five distinct regions. From head to tail, these include the truncus arteriosus, bulbus cordis, primitive ventricle, primitive atrium, and the sinus venosus. Initially, all venous blood flows into the sinus venosus, and contractions propel the blood from tail to head, or from the sinus venosus to the truncus arteriosus. This is a very different pattern from that of an adult.
Figure.17.Embryonic Development of the Heart.
A healthy adult has a resting heart rate (pulse) of 60 to 80 beats per minute, which is the rate of depolarization of the SA node. (The SA node actually has a slightly faster rate, closer to 100 beats per minute, but is slowed by parasympathetic nerve impulses to what we consider a normal resting rate.) A rate less than 60 (except for athletes) is called bradycardia; a prolonged or consistent rate greater than 100 beats per minute is called tachycardia.
A child’s normal heart rate may be as high as 100 beats per minute, that of an infant as high as 120, and that of a near-term fetus as high as 140 beats per minute. These higher rates are not related to age, but rather to size: the smaller the individual, the higher the metabolic rate and the faster the heart rate. Parallels may be found among animals of different sizes; the heart rate of a mouse is about 200 beats per minute and that of an elephant about 30 beats per minute. well-conditioned athletes have low resting pulse rates. Those of basketball players are often around 50 beats per minute, and the pulse of a marathon runner often ranges from 35 to 40 beats per minute. When our skeletal muscles are exercised, they become stronger and more efficient. The same is true for the heart; consistent exercise makes it a more efficient pump, as you will see in the next section.
The Conduction System of the Heart
The cardiac cycle is regulated by specialized areas in the heart wall that forms the conduction system of the heart. Two of these areas are tissue mass called nodes; the third is a group of fibers called the atrioventricular bundle. The sinoatrial node, which is located I the upper wall of the right atrium an initiates the heart beat, is called the pacemaker. The second node, located in the ineratrial septum at the bottom of the right atrium, is called the atrioventricular node. The atrioventricular bundle, also known as the bundle of His, is located at the top of the interventricular septum; it has branches that extend to all parts of the ventricle walls. Fibers travel first down both sides of the interventricular septum in groups called the right and left bundle branches. Smaller Purkinje fibers then travel in a branching network throughout the myocardium of the ventricles . The order in which the impulses travel is as follows:
- The sinoatrial node generates the electric impulse that begins the heart beat.
- The excitation wave travels throughout the muscle of each atrium, causing it to contract.
- The atrioventricular node is stimulated.The relatively slower conduction through this node allows time for the atria to contract and complete the filling of the ventricles.
- The excitation wave travels rapidly through the bundle of His and then throughout the ventricular walls by means of the bundle branches and Purkinje fibers. The entire musculature of the ventricles contracts practically at once. As a safety measure, a region of the conduction system other than the sinoatrial node fails, but it does so at a slower rate.
Factors affecting heart rate.
- Body temperature. Higher body temperature results in an increased heart rate; a lower body temperature reduces the heart rate.
- Emotions. Excitement, anger, anxiety, and fright, for example, all cause the heart to beat faster. Depression and grief can decrease the heart rate.
- Chemicals.Chemicals present in the blood (such as hormones) affect the heart rate, as do chemicals taken as drugs.
- Age. Our resting heart rates gradually slow down as we get older.
- Gender. Men tend to have lower heart rates than women, with 70–72 beats per minute compared to 78–82 for women.
- Activity. Vigorous exercise, for example, increases the heart rate; during periods of relaxation the heart rate slows down.
- Physical condition.The resting heart rate of people who exercise tends to be lower than that of the inactive. Blood pressure Stimuli affecting blood pressure in general also affect heart rate.
- Heart disease. Various diseases and disorders of the heart can affect heart rate.
- The heart rate is also affected by such factors as hormones, ions, and drugs in the blood.
Bradycardia is a relatively slow heart rate of less than 60 beats/minute.
During rest and sleep, the heart may beat less than 60 beats/minute but usually does not fall below 50 beats/minute.
- Tachycardia refers to a heart rate over 100 beats/minute.
- Sinus arrhythmia is a regular variation in heart rate due to changes in the rate and depth of breathing. It is normal phenomenon.
- Premature beats, also called extrasystoles are beats that come in before the the expected normal beats. They may occur in normal persons initiated by caffeine, nicotine, or psycologic stresses. They are also common in persons with heart disease.
Regualation of the Heart rate.
Although the heart generates and maintains its own beat, the rate of contraction can be changed to adapt to different situations. Although the fundamental beat of the heart originates within the heart itself, the heart rate can be influenced by the nervous system and by other factors in the internal environment. These influences allow the heart to meet changing need rapidly. The nervous system can and does bring about necessary changes in heart rate as well as in force of contraction. The medulla of the brain contains the two cardiac centers, the accelerator center and the inhibitory center.These centers send impulses to the heart along autonomic nerves.
Figure.18.Nervous regulation of the heart.
Venous drainage refers to the route by which blood leaves an organ. After flowing through capillaries of the heart wall, about 20% of the coronary blood empties directly from multiple small thebesian13 veins into the right ventricle. The other 80% returns to the right atrium by the following route
Membrane that encases the heart (peri means around) (cardium relates to heart). The heart is enclosed in a double-walled sac called the pericardium. The outer wall, called the parietal pericardium (pericardial sac), has a tough, superficial fibrous layer of dense irregular connective tissue and a deep, thin serous layer. The serous layer turns inward at the base of the heart and forms the visceral pericardium (epicardium) covering the heart surface . The pericardial sac is anchored by ligaments to the diaphragm below and the sternum anterior to it, and more loosely anchored by fibrous connective tissue to mediastinal tissue dorsal to the heart. Pericardium contracts and relaxes to force blood to move through the circulatory system.
The conducting system.
An important role in the rhythmic work of the heart and in the coordination of the activity of the musculature of the separate heart chambers is played by the conducting system of the heart. Although the atrial musculature is separated from the ventricular musculature by fibrous rings, the two musculatures are, nevertheless, connected by the conducting system, which is composed of a complex of special cardiac muscles fibres (fibres of Purkinje). The cells of these muscle fibres are poor in myofibrils but rich in sarcoplasm. The following nodes and bundles are distinguished in the conducting system:
- The sinoatrial node (nodus sinuatrialis) or Keith-Flack’s sinoatrial bundle is located in an area of the right atrial wall in sulcus terminalis, between the superior vena cava and the right auricle. It is connected with the musculature of the atria and is important for their rhythmic contraction. The atria are, therefore, connected to each other by the sinoatrial bundle and to the ventricles by the atrioventricular bundle. Stimulation from the right atrium is usually conducted from the sinoatrial node to the atrioventricular node.
- The atrioventricular bundle (fasciculus atrioventricularis) arises as a thickening of the atrioventricular node, nodus atrioventricularis (the node of Aschoif and Tawara), lying in the wall of the right atrium near the cuspis septalis of the tricuspid valve. The fibres of the node are directly connected with the atrial musculature and continue into the septum between the ventricles as the atrioventricular bundle of His. In the septum between the ventricles, the bundle of His divides into right and left crura (crus dextrum and crus sinistrum), which pass into the walls of the respective ventricles and give off branches under the endocardium in the musculature. The atrioventricular bundle is significant in the work of the heart since it conducts the wave of contraction from the atria to the ventricles that regulates the rhythm of the systole of the atria and ventricles. The sinoatrial and atrioventricular bundles should be considered a neuromuscular complex, which is connected with all parts of the heart and with the central nervous system.
Partitions of human Heart.
Physicians often refer to the right heart and the left heart. This is because the human heart is really a double pump. The two sides are completely separated from each other by a partition called the septum. The upper part of this partition is called interartrial septum; while the larger the lower portion is called interventricular septum. The septum, like the heart wall, consists largely of myocardium.
The vessels of the heart.
There are three principal categories of blood vessels—arteries, veins, and capillaries. Arteries are the efferent vessels of the cardiovascular system that is, vessels that carry blood away from the heart. Veins are the afferent vessels—vessels that carry blood back to the heart. Capillaries are microscopic, thin-walled vessels that connect the smallest arteries to the smallest veins. Aside from their general location and direction of blood flow, these three categories of vessels also differ in the histological structure of their walls.
The Vessel Wall.
The walls of arteries and veins are composed of three layers called tunics.
- The tunica interna (tunica intima) lines the inside of the vessel and is exposed to the blood. It consists of a simple squamous epithelium called the endothelium, overlying a basement membrane and a sparse layer of loose connective tissue. The endothelium acts as a selectively permeable barrier to materials entering or leaving the bloodstream; it secretes chemicals that stimulate the muscle of the vessel wall to contract or relax, thus narrowing or widening the vessel; and it normally repels blood cells and platelets so that they flow freely without sticking to the vessel wall. When the endothelium is damaged, however, platelets may adhere to it and form a blood clot; and when the tissue around a vessel is inflamed, the endothelial cells produce cell-adhesion molecules that induce leukocytes to adhere to the surface. This causes leukocytes to congregate in tissues where their defensive actions are needed.
- The tunica media, the middle layer, is usually the thickest. It consists of smooth muscle, collagen, and in some cases, elastic tissue. The relative amounts of smooth muscle and elastic tissue vary greatly from one vessel to another and form a basis for classifying vessels as described in the next section. The principal functions of the tunica media are to strengthen the vessels and prevent the blood pressure from rupturing them, and to provide for vasomotion, changes in the diameter of a blood vessel. The widening of a vessel is called vasodilation and a narrowing is called vasoconstriction.
- The tunica externa is the outermost layer. It consists of loose connective tissue that often merges with that of neighboring blood vessels, nerves, or other organs. It anchors the vessel and provides passage for small nerves, lymphatic vessels, and smaller blood vessels. Small vessels called the vasa vasorum supply blood to at least the outer half of the wall of a larger vessel. Tissues of the inner half of the wall are thought to be nourished by diffusion from blood in the lumen.
Arteries are sometimes called the resistance vessels of the cardiovascular system because they have a relatively strong, resilient tissue structure that resists the high blood pressure within. Each beat of the ventricles creates a surge of pressure in the arteries as blood is ejected into them. Arteries are constructed to withstand these pressure surges. They are more muscular than veins, so they retain their round shape even when empty, and they appear relatively circular in tissue sections. The arteries of the heart, the right and left coronary arteries (a. coronaria dextra and a. coronaria sinistra) arise from the bulbus aortae below the superior margins of the semilunar valves. As a result, during systole the entrance to the coronary arteries is closed by the valves, while the arteries themselves are compressed by the contracted heart muscles. As a consequence, the supply of blood to the heart diminishes during systole; blood enters the coronary arteries during diastole when the openings of these arteries in the orifice of the aorta are not closed by the semilunar valves.
The right coronary artery (a. coronaria dextra) arises from the aorta corresponding to the right semilunar valvule and passes between the aorta and the auricle of the right atrium laterally. From there it curves around the right border of the heart in the coronary sulcus and passes over to its posterior surface. Here it is continuous with the interventricular branch (ramus interventricularis posterior). Along the right margine is located marginal branch. The interventricular branch descends in the posterior interventricular sulcus to the heart apex where it anastomoses with the branch of the left coronary artery.
The branches of the right coronary artery vascularize: the right atrium, part of the anterior and the entire posterior wall of the right ventricle, a small area of the posterior wall of the left ventricle, the interatrial septum, the posterior one-third of the interventricular septum, the papillary muscles of the right ventricle, and the posterior papillary muscle of the left ventricle.
The left coronary artery (a. coronaria sinistra) arises from the aorta at the left similunar valvule and also lies in the coronary sulcus to the front of the left atrium. Between the pulmonary trunk and the left auricle, it gives off two branches: a thinner, anterior interventricular branch (ramus interventricularis anterior) and a larger, left circumflex branch (ramus circumflexus). The first descends along the anterior interventricular sulcus to the heart apex where it anastomoses with the branch of the right coronary artery. The second is a continuation of the main trunk of the left coronary artery; it curves around the heart from the left side in the coronary sulcus and is also connected with the right coronary artery. As a result, an arterial ring forms along the whole coronary sulcus, which is located in a horizontal plane and from which branches to the heart rise perpendicularly. The ring is a functional adaptation for the collateral circulation of the heart. The branches of the left coronary artery vascularize the left atrium, the entire anterior and the greater part of the posterior left ventricular wall, part of the anterior wall of the right ventricle, the anterior two-thirds of the interventricular septum, and the anterior papillary muscle of the left ventricle.
Developmental variants of the coronary arteries may occur, as a result of which the correlations of the blood-supply channels differ. Three forms of blood supply to the heart are distinguished from this standpoint: uniform blood supply, with similar development of both coronary arteries, left-coronary blood supply, and right-coronary blood supply. In addition to the coronary arteries, arteries reach the heart from the bronchial arteries, from the inferior surface of the aortic arch near the arterial ligament. These arteries must be considered during operations on the lungs and oesophagus since injury to them would adversely affect blood supply to the heart. The intraorganic arteries of the heart. According to the four heart chambers, the coronary arteries and their large branches give off arteries to the atria (aa. atriales) and their auricles (aa. auriculares), the ventricles (aa. ventriculares), and the septa between them (aa. septi anterior and septi posterior). On penetrating the thickness of the myocardium, they branch out according to the number, location, and structure of its layers: first in the outer layer, then in the middle layer (in the ventricles), and finally in the inner layer, after which they penetrate the papillary muscles (aa. papillares) and even the atrio-ventricular valves. The intramuscular arteries, in each layer follow the course of the muscle bundles and anastomose in all the layers and sections of the heart. The walls of some of these arteries have a strongly developed layer of smooth muscles, which contract to close the lumen of the vessel completely. The arteries are, therefore, called “closing” arteries. Temporary spasm of these arteries may lead to the cessation of the flow of blood to the given area of the heart muscle and cause myocardial infarction. Some branches pass through muscular fibers that also compress them during ventricular systole (muscular bridge). A case of an accessory coronary artery of the heart arising from the pulmonary trunk has been described.
The Division of Ateries.
The Arteries as the blood vessels are divided into three categories by size, but of course there is a smooth transition from one category to the next.As follows.
- Conducting (elastic or large) arteries are the biggest arteries. The aorta, common carotid and subclavian arteries, pulmonary trunk, and common iliac arteries are examples of conducting arteries. There is a very thin layer of elastic fibers called the internal elastic lamina at the border between the intima and media, but it is sparse and not very visible microscopically. The tunica media consists of 40 to 70 layers of elastic sheets, perforated like slices of Swiss cheese, alternating with thin layers of smooth muscle, collagen, and elastic fibers. In histological sections, the view is dominated by this elastic tissue. There is a thin external elastic lamina at the border between the media and externa. The tunica externa is relatively thick and well supplied with vasa vasorum. Conducting arteries expand during ventricular systole to receive blood, and recoil during diastole. Their expansion takes some of the pressure off the blood so that smaller arteries downstream are subjected to less systolic stress. Their recoil between heartbeats prevents the blood pressure from dropping too low while the heart is relaxing and refilling. These effects lessen the fluctuations in blood pressure that would otherwise occur. Arteries stiffened by atherosclerosis cannot expand and recoil as freely. Consequently, the downstream vessels are subjected to greater stress and are more likely to develop aneurysms and rupture.
- Distributing (muscular or medium) arteries are smaller branches that distribute blood to specific organs. You could compare a conducting artery to an interstate highway and distributing arteries to the exit ramps and state highways that serve specific towns. Most arteries that have specific anatomical names are in these first two size classes. The brachial, femoral, renal, and splenic arteries are examples of distributing arteries. Distributing arteries typically have up to 40 layers of smooth muscle constituting about three-quarters of the wall thickness. This smooth muscle is more conspicuous than the elastic tissue in histological specimens of distributing arteries. Both the internal and external elastic laminae, however, are thick and often histologically conspicuous in distributing arteries.
Hepatic Portal System.
Almost always, when blood leaves a capillary bed it returns directly to the heart. In a portal system, however, blood circulates through a second capillary bed, usually in a second organ, before returning to the heart. Thus, a portal system is a kind of detour in the pathway of venous return that can transport materials directly from one organ to another. The portal system between the hypothalamus and the anterior pituitary has already been described. The largest portal system in the body is the hepatic portal system, which carries blood from the abdominal organs to the liver.
The hepatic portal system includes the veins drains blood from capillaries in the spleen, stomach, pancreas, and intestine. Instead of emptying their blood directly into the inferior vena cava, they deliver it by way of the hepatic portal vein to the liver. The largest tributary of the portal vein is the superior mesenteric vein it is joined by the spleenic vein just under the liver. Other tributaries of the portal circulation are the gastric, pancreatic, and inferior mesenteric veins.
The natural pacemaker of the heart is the sinoatrial (SA) node, a specialized group of cardiac muscle cells located in the wall of the right atrium just below the opening of the superior vena cava. The SA node is considered specialized because it has the most rapid rate of contraction, that is, it depolarizes more rapidly than any other part of the myocardium (60 to 80 times per minute). As you may recall, depolarization is the rapid entry of Na ions and the reversal of charges on either side of the cell membrane. The cells of the SA node are more permeable to Na ions than are other cardiac muscle cells. Therefore, they depolarize more rapidly, then contract and initiate each heartbeat. From the SA node, impulses for contraction travel to the atrioventricular (AV) node, located in the lower interatrial septum. The transmission of impulses from the SA node to the AV node and to the rest of the atrial myocardium brings about atrial systole.
Nerve Supply to the Heart.
Even though the heart has its own pacemaker, it does receive both sympathetic and parasympathetic nerves, which modify the heart rate and contraction strength. Sympathetic stimulation is able to raise the heart rate to as high as 230 beats/min, while parasympathetic stimulation can slow the heart rate to as low as 20 beats/min or even stop the heart for a few seconds. The sympathetic pathway to the heart originates with neurons in the lower cervical to upper thoracic spinal cord. Efferent fibers from these neurons pass from the spinal cord to the sympathetic chain and travel up the chain to the three cervical ganglia. Cardiac nerves arise from the cervical ganglia (see fig. 16.4) and lead mainly to the ventricular myocardium, where they increase the force of contraction. Some fibers, however, innervate the atria.
Sympathetic fibers to the coronary arteries dilate them and increase coronary blood flow during exercise. The parasympathetic pathway to the heart is through the vagus nerves. The right vagus nerve innervates mainly the SA node and the left vagus nerve innervates mainly the AV node, although there is some cross-innervation from each nerve to both nodes. The ventricles receive little or no vagal stimulation. The vagus nerves slow the heartbeat. Without this influence, the SA node would produce an average resting heart rate of about 100 beats/min, but steady background firing of the vagus nerves (vagal tone) normally holds the resting rate down to about 70 to 80 beats/min.
The nerves innervating the heart musculature, with its distinctive structure and function, are complex and form numerous plexuses. The whole nervous system of the heart is composed of: 1) arriving nerve trunks; 2) plexuses in the heart itself; and 3) plexuses connected with those of the ganglionic fields. The nerves of the heart are divided according to function into four types (I.P. Pavlov): decelerating, accelerating, diminishing, and intensifying. Morphologically they are part of the vagus nerve and the sympathetic trunk. The sympathetic nerves (mainly the postganglionic fibres) branch off from the upper three cervical and upper five thoracic sympathetic ganglia: n. cardiacus cervicalis superior from the ganglion cervicale superius; n. cardiacus cervicalis medius from the ganglion cervicale medium; n. cardiacus cervicalis inferior from the ganglion cervicale inferius or ganglion cervicothoracicum s. ganglion stellatum, and nn. cardiaci thoraciii from the thoracic ganglia of the sympathetic trunk. When there are four cervical ganglia, a fourth rt. cardiacus cervicalis exists; in individuals with two cervical ganglia, there are only two cervical cardiac nerves.
The cardiac branches of the vagus nerve (parasympathetic) arise from its cervical (rami cardiaci superiores) and thoracic (rami cardiaci medii) parts and from n. laryngeus recurrens vagi (rami cardiaci inferiores). The arriving nerves are composed of two groups, superficial and deep. The superficial group adjoins the carotid and subclavian arteries in the superior segment and the aorta and pulmonary trunk in the inferior segment. The deep group, composed mainly of vagal branches, lies on the anterior surface of the lower third of the trachea. These branches come in contact with the lymph nodes in the region of the trachea. If these nodes become enlarged, e.g., in pulmonary tuberculosis, they may compress the vagal branches, which lead to changes in the heart rhythm. Two nerve plexuses form from the sources mentioned: a superficial plexus, plexus cardiacus superficialis, between the arch of the aorta (under it) and the bifurcation of the pulmonary trunk; a deep plexus, plexus cardiacus profundus, between the arch of the aorta (behind it) and the bifurcation of the trachea.
These plexuses are continuous with the plexus coronarius dexter and the plexus coronarius sinister surrounding the vessels of the same name, as well as with the plexus located between the epicardium and myocardium. The latter plexus gives off intraorganic branches of nerves. Numerous groups of ganglionic cells, nerve ganglia, are contained in the plexuses. Six intracardiac plexuses located under the epicardium are distinguished: two anterior plexuses (the first on the left, the second on the right) descend along the aorta and pulmonary trunk to the ventricles; there are two posterior plexuses, one on the border between the atria (the third) and the other on the posterior wall of the ventricles (the fourth); the fifth plexus is on the anterior wall of the atria and the sixth on the posterior wall of the left atrium. All plexuses are attended by ganglionic fields which occupy, as do the plexuses, a definite territory, although the number of ganglia forming them, their size, and their interrelationship often vary. The ganglionic fields are most highly developed in man.
The fetus depends upon the mother for oxygen and nutrients and for the removal of carbon dioxide and other waste products. The site of exchange between fetus and mother is the placenta, which contains fetal and maternal blood vessels that are very close to one another. The blood of the fetus does not mix with the blood of the mother; substances are exchanged by diffusion and active transport mechanisms passes through the ductus venosus to the inferior vena cava, to the right atrium. After birth, when the umbilical cord is cut, the remnants of these fetal vessels constrict and become nonfunctional.
The fit and unfit heart.
The diagram below shows the comparative amounts of work done by a fit heart and an unfit heart during various activities. The higher the heart rate, the harder the heart is having to work; when the heart rate is low, the heart is being used efficiently. The unfit heart has to work much harder all the time, and so may be under a constant strain. A healthy heart works under a self-imposed maximum pulse rate of about 190 beats per minute, which means that even under severe, unplanned stress it is unlikely to increase its work to a dangerously fast rate.
The following are examples of Heart dissoders.
- Angina pectoris Pain or discomfort in the chest.This is heart dissoder is caused by inadequate oxygen supply to the heart, sometimes as a result of narrowed coronary arteries. Angina its often happens during exercise or stress.
- Arrhythmia. This is an abnormal heart rate or rhythm caused by a disruption of the heart’s conduction system, which generates and transmits electrical impulses in the heart. It can be caused by coronary artery disease, stress, exertion, or some drugs.
- Bradycardia. A slow heart rate—below 60 beats a minute.
- Cardiomegaly .Enlargement of the heart. There are a number of causes.
- Congenital heart defects. Heart defects in newborn babies including: ventricular septal defect (the wall between two ventricles does not form properly), coarctation of the aorta (the aorta is narrowed), pulmonary stenosis (the pulmonary semilunar valve is narrowed), and tetralogy of Fallot (multiple defects).
- Cor pulmonale. Disease of the heart caused by disease of the blood vessels to the lungs or disease of the lungs themselves.
- Endocarditis Inflammation of the endocardium (inner heart lining) often resulting from infection by bacteria.
- Epicarditis. Inflammation of the epicardium (outer lining of the heart).
- Fibrillation. Rapid, irregular contractions of the heart.
- Heart block .Electrical impulses in the heart are blocked at points in the conduction system.
- Heart failure. The heart pumps less blood than the body needs and so is not capable of supplying the oxygen demands of the tissues. Results in congestion of blood and lack of nutrition to tissues.
- Mitral valve prolapse. Improper closure of the mitral valve (the valve between the left atrium and ventricle). Also called floppy valve syndrome.
- Myocardial infarction Commonly called heart attack, a condition in which obstruction of blood flowing to the heart muscle results in tissue death. It is most often caused by atherosclerosis of the coronary arteries.
- Palpitations. Rapid or irregular heartbeat caused by drugs, emotions, or heart disorders.
- Pericarditis. Inflammation of the bag (pericardium) that encloses the heart. Too much fluid may be produced in the pericardial space, so that the heart is compressed and unable to fill properly. The two layers of the pericardium become stuck together, restricting the heart’s movement.
- Pulmonary atresia A complete blockage between the heart and the main pulmonary artery.
- Stokes-Adams syndrome. A sudden attack of unconsciousness accompanying heart block.
- Tachycardia. A fast heart rate which is above 100 beats a minute. Tricuspid atresia The heart has no tricuspid valve; the right ventricle is usually small. There is a reduced flow of blood to the lungs.
- Valvular stenosis.Narrowing of a heart valve, which causes the heart to work harder to push blood around the body
The term “heart attack” is usually used to describe a sudden blockage in a heart artery. A more accurate term is “myocardial infarction” (MI). If a heart artery is blocked for more than a few minutes, the muscle cells (myocardium) may become permanently damaged. If the amount of muscle damage is small, there will be enough good muscle left for the heart to work again once the heart attack is over. Heart attacks can start at any time of the day or night, when a person is resting or being active. Sometimes, a heart attack can be brought on by unusually energetic activity or by massive stress. People with a family history of heart attacks may be more likely to have a heart attack themselves. People with diabetes are also more likely to have heart problems although the reason for this is not clear.Heart attacks occur more often in men than women and mostly in people over 40.
The impacts of Smoking on Heart
Medical research has proved that smoking constitutes a grave health risk, with more and more diseases proving to be associated with, or aggravated by, smoking. Women who smoke while pregnant can cause damage to their babies. If a smoker continues to smoke after a heart attack, this doubles their risk of having another heart attack within one year. The risk of having a heart attack starts to reduce as soon as a person gives up smoking, and is half as likely to happen within one year of stopping smoking. Advice on giving up smoking can be obtained from doctors, nurses, and pharmacists, as well as “stop-smoking” help groups.
The most common reason for heart arteries to become blocked is due to a buildup of layers of fatty material (cholesterol) inside the arteries. The walls of these damaged arteries may crack and a blood clot may form on top of the crack. This can suddenly block off the artery completely. Occasionally, the blockage is caused by a spasm of the muscle walls of the coronary arteries. It can also be due to a very fast heart rate, when the heart muscle demands more oxygen than the blood supply can provide. Heart attacks cause severe pain and other symptoms such as sweating, nausea, or shortness of breath.
As a humans we are faced by the various Heart problems which led to the decrease of heart rate.The following are some of the Heart problems.
- Congenital malformations. Babies can be born with heart problems, sometimes involving a hole in the wall between the chambers of the heart.
- Diseases of the valves. These can either be congenital, or the result of disease or infection.
- Diseases of the blood vessels. Deposits of fat can be laid down within the walls of the vessels, usually the larger arteries. This is often associated with a raised cholesterol and fat level in the blood.
- Coronary artery problems. The heart gains its blood supply by a system of vessels called the coronary artery circulation. Like the other arteries, this may have fatty deposits in the walls; if the deposits completely block the vessel then a heart attack results. The area of the heart muscle supplied by that vessel is starved of oxygen and dies. If this process happens to vessels that supply the brain with blood, then a stroke is the result. There are various factors that make heart attacks more likely. The most important ones to be avoided are cigarette smoking, raised blood pressure, being overweight, lack of exercise, and stress.
- Scar from an old heart attack. If a heart attack occurs the scar is permanent, but by avoiding the factors that make heart attacks more likely, the damage can be minimized.
- Problems with the heart muscle. The heart is a muscular pump; if the blood pressure is raised, which may happen for a variety of reasons (such as kidney disease), the heart enlarges and the valves may work inefficiently. The increase in pressure within the blood vessels may cause damage to the anatomy of the vessel walls and cause a rupture. The most frequent site for this is within the skull, and a stroke is the result.
- Problems with the heart pacemaker. The heart beats in response to small electrical impulses arising in a bundle of nerve fibers at the center of the heart. If this pacemaker is not functioning correctly, disturbances of the rhythm of the heart result.
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