However, the excess fluid in the pericardial cavity puts pressure on the heart and prevents full relaxation, so the chambers within the heart contain slightly less blood as they begin each heart cycle. Over time, less and less blood is ejected from the heart. If the fluid builds up slowly, as in hypothyroidism, the pericardial cavity may be able to expand gradually to accommodate this extra volume.
Some cases of fluid in excess of one liter within the pericardial cavity have been reported. Rapid accumulation of as little as mL of fluid following trauma may trigger cardiac tamponade. Other common causes include myocardial rupture, pericarditis, cancer, or even cardiac surgery. Removal of this excess fluid requires insertion of drainage tubes into the pericardial cavity.
Premature removal of these drainage tubes, for example, following cardiac surgery, or clot formation within these tubes are causes of this condition. Untreated, cardiac tamponade can lead to death.
Inside the pericardium, the surface features of the heart are visible, including the four chambers. Auricles are relatively thin-walled structures that can fill with blood and empty into the atria or upper chambers of the heart. You may also hear them referred to as atrial appendages. 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. Figure 5 illustrates anterior and posterior views of the surface of the heart.
Figure 5. Inside the pericardium, the surface features of the heart are visible. The wall of the heart is composed of three layers of unequal thickness. From superficial to deep, these are the epicardium, the myocardium, and the endocardium. The outermost layer of the wall of the heart is also the innermost layer of the pericardium, the epicardium, or the visceral pericardium discussed earlier.
Figure 6. The middle and thickest layer is the myocardium , made largely of cardiac muscle cells. It is built upon a framework of collagenous fibers, plus the blood vessels that supply the myocardium and the nerve fibers that help regulate the heart.
It is the contraction of the myocardium that pumps blood through the heart and into the major arteries. The muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart. They form a figure 8 pattern around the atria and around the bases of the great vessels. Deeper ventricular muscles also form a figure 8 around the two ventricles and proceed toward the apex. More superficial layers of ventricular muscle wrap around both ventricles.
This complex swirling pattern allows the heart to pump blood more effectively than a simple linear pattern would. Figure 6 illustrates the arrangement of muscle cells.
Although the ventricles on the right and left sides pump the same amount of blood per contraction, the muscle of the left ventricle is much thicker and better developed than that of the right ventricle. In order to overcome the high resistance required to pump blood into the long systemic circuit, the left ventricle must generate a great amount of pressure. The right ventricle does not need to generate as much pressure, since the pulmonary circuit is shorter and provides less resistance.
The image below illustrates the differences in muscular thickness needed for each of the ventricles. Figure 7. The myocardium in the left ventricle is significantly thicker than that of the right ventricle. Both ventricles pump the same amount of blood, but the left ventricle must generate a much greater pressure to overcome greater resistance in the systemic circuit.
The ventricles are shown in both relaxed and contracting states. Note the differences in the relative size of the lumens, the region inside each ventricle where the blood is contained. The innermost layer of the heart wall, the endocardium , is joined to the myocardium with a thin layer of connective tissue.
The endocardium lines the chambers where the blood circulates and covers the heart valves. It is made of simple squamous epithelium called endothelium , which is continuous with the endothelial lining of the blood vessels.
Once regarded as a simple lining layer, recent evidence indicates that the endothelium of the endocardium and the coronary capillaries may play active roles in regulating the contraction of the muscle within the myocardium. The endothelium may also regulate the growth patterns of the cardiac muscle cells throughout life, and the endothelins it secretes create an environment in the surrounding tissue fluids that regulates ionic concentrations and states of contractility.
Endothelins are potent vasoconstrictors and, in a normal individual, establish a homeostatic balance with other vasoconstrictors and vasodilators. In order to develop a more precise understanding of cardiac function, it is first necessary to explore the internal anatomical structures in more detail. 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. 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 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 interventricular septum is visible in the image below. In this figure, the atrioventricular septum has been removed to better show the bicupid and tricuspid 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. Figure 8. This anterior view of the heart shows the four chambers, the major vessels and their early branches, as well as the valves.
The presence of the pulmonary trunk and aorta covers the interatrial septum, and the atrioventricular septum is cut away to show the atrioventricular valves. One very common form of interatrial septum pathology is patent foramen ovale, which occurs when the septum primum does not close at birth, and the fossa ovalis is unable to fuse. As much as 20—25 percent of the general population may have a patent foramen ovale, but fortunately, most have the benign, asymptomatic version.
Patent foramen ovale is normally detected by auscultation of a heart murmur an abnormal heart sound and confirmed by imaging with an echocardiogram. Despite its prevalence in the general population, the causes of patent ovale are unknown, and there are no known risk factors. In nonlife-threatening cases, it is better to monitor the condition than to risk heart surgery to repair and seal the opening. Coarctation of the aorta is a congenital abnormal narrowing of the aorta that is normally located at the insertion of the ligamentum arteriosum, the remnant of the fetal shunt called the ductus arteriosus.
If severe, this condition drastically restricts blood flow through the primary systemic artery, which is life threatening. In some individuals, the condition may be fairly benign and not detected until later in life. Detectable symptoms in an infant include difficulty breathing, poor appetite, trouble feeding, or failure to thrive.
In older individuals, symptoms include dizziness, fainting, shortness of breath, chest pain, fatigue, headache, and nosebleeds. Treatment involves surgery to resect remove the affected region or angioplasty to open the abnormally narrow passageway.
Studies have shown that the earlier the surgery is performed, the better the chance of survival. A patent ductus arteriosus is a congenital condition in which the ductus arteriosus fails to close. The condition may range from severe to benign.
Failure of the ductus arteriosus to close results in blood flowing from the higher pressure aorta into the lower pressure pulmonary trunk. This additional fluid moving toward the lungs increases pulmonary pressure and makes respiration difficult. Symptoms include shortness of breath dyspnea , tachycardia, enlarged heart, a widened pulse pressure, and poor weight gain in infants. Treatments include surgical closure ligation , manual closure using platinum coils or specialized mesh inserted via the femoral artery or vein, or nonsteroidal anti-inflammatory drugs to block the synthesis of prostaglandin E2, which maintains the vessel in an open position.
If untreated, the condition can result in congestive heart failure. Septal defects are not uncommon in individuals and may be congenital or caused by various disease processes. Tetralogy of Fallot is a congenital condition that may also occur from exposure to unknown environmental factors; it occurs when there is an opening in the interventricular septum caused by blockage of the pulmonary trunk, normally at the pulmonary semilunar valve. This allows blood that is relatively low in oxygen from the right ventricle to flow into the left ventricle and mix with the blood that is relatively high in oxygen.
Symptoms include a distinct heart murmur, low blood oxygen percent saturation, dyspnea or difficulty in breathing, polycythemia, broadening clubbing of the fingers and toes, and in children, difficulty in feeding or failure to grow and develop. It is the most common cause of cyanosis following birth. Other heart defects may also accompany this condition, which is typically confirmed by echocardiography imaging.
Tetralogy of Fallot occurs in approximately out of one million live births. Normal treatment involves extensive surgical repair, including the use of stents to redirect blood flow and replacement of valves and patches to repair the septal defect, but the condition has a relatively high mortality. Survival rates are currently 75 percent during the first year of life; 60 percent by 4 years of age; 30 percent by 10 years; and 5 percent by 40 years.
Septal defects are commonly first detected through auscultation, listening to the chest using a stethoscope. In this case, instead of hearing normal heart sounds attributed to the flow of blood and closing of heart valves, unusual heart sounds may be detected.
This is often followed by medical imaging to confirm or rule out a diagnosis. In many cases, treatment may not be needed. Some common congenital heart defects are illustrated in Figure 9. Figure 9. The right atrium serves as the receiving chamber for blood returning to the heart from the systemic circulation. The two major systemic veins, the superior and inferior venae cavae, and the large coronary vein called the coronary sinus that drains the heart myocardium empty into the right atrium.
The superior vena cava drains blood from regions superior to the diaphragm: the head, neck, upper limbs, and the thoracic region. The impulse is then distributed through the Purkinje fibers subendocardial branches , which transmit the signal to papillary muscles and the ventricular wall. Coordinated contraction of the ventricles begins at the apex and moves toward the base. The rate chronotropic and force inotropy of cardiac contractions are regulated through sympathetic and parasympathetic innervation.
Cell bodies for sympathetic innervation are located within the first 5 thoracic levels of the spinal cord while parasympathetic innervation works through branches of the vagus nerve CN X. The fibrous pericardium and serous pericardium are innervated by the phrenic nerve, which is derived primarily from cervical nerve 4 but also has contributions from the 3 and 5.
Due to its origin, pericarditis and other cardiac complications can cause referred pain to the shoulder. The serous pericardium has branches of innervation from the vagus nerve via the esophageal plexus. The pericardium has an extensive set of mechanoreceptors and chemoreceptors that are responsible for certain reflexes. The Bezold-Jarisch reflex refers to a triad of bradycardia, hypotension, and apnea that occurs due to receptors in this area.
Moving superficially, the heart wall can be divided into the endocardium, myocardium, and epicardium. The endocardium is a thin layer of supporting connective tissue and smooth muscle fibers, which line the heart chambers and valves.
The myocardium is the thickest of the three layers, particularly within the left ventricle, and is responsible for the ejection of blood during contractions. The epicardium visceral pericardium is responsible for the production of pericardial fluid and the protection of the other heart layers. Dextrocardia refers to the congenital condition where the apex of the heart is directed toward the right side of the chest.
The defect is often attributed to Kartagener syndrome primary ciliary dyskinesia. A patent foramen ovale occurs if the septum primum and septum secundum fail to fuse during embryogenesis. This can lead to paradoxical emboli that enter systemic circulation instead of the lungs.
Tetralogy of Fallot TOF is a congenital heart defect due to the anterior deviation of the aorticopulmonary septum. The malalignment leads to pulmonary stenosis, an overriding aorta, a ventricular septal defect, and right ventricular hypertrophy. Ventricular septal defects are the most common congenital cardiac anomaly. They often occur within the membranous portion of the ventricular septum and can lead to a left-to-right shunt within the newborn.
While the pericardium serves many physiological roles, its presence is not a necessity. Congenital absence of the pericardium or its surgical removal pericardiectomy does not tend to cause symptoms in patients. They can occasionally compress cardiac structures, such as coronary arteries or the left atrial appendage.
Coronary artery bypass grafting CABG is a procedure to restore cardiac tissue perfusion after a coronary artery becomes occluded. Pericardiocentesis is a medical procedure where the fluid is aspirated from the pericardial cavity. Typically, the needle is inserted just left of the xiphoid process and inferior to the left costal margin. Echocardiography is often utilized to prevent puncturing the heart.
Due to their location on each side of the pericardium, phrenic nerves must be identified during thoracic surgeries. Associated Conditions. The Mesothelium The parietal and visceral layers are both made up of mesothelium , which is comprised of epithelial cells.
The two main functions of mesothelium are to: Form a protective barrier Provide a frictionless surface for free movement of organs and tissues. Was this page helpful? Thanks for your feedback! Sign Up. What are your concerns? Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
Related Articles. What Causes JVD? The Heart: Anatomy, Function, and Conditions. Pericarditis Refers to Inflammation of the Heart Lining. Causes of Right Side Chest Pain. What Are the Causes of Cardiac Tamponade? The Anatomy of the Superior Vena Cava. The Anatomy of the Subclavian Artery. The Anatomy of the Subclavian Vein. The Anatomy of the Uterus. The pericardium is a thin sac that surrounds your heart. It protects and lubricates your heart and keeps it in place within your chest.
Problems can occur when the pericardium becomes enflamed or fills with fluid. The swelling can damage your heart and affect its function. In between these two layers is the fluid-filled pericardial cavity. It lubricates the heart and protects it from injury. Pericardial effusion is the buildup of too much fluid between the pericardium and your heart.
This can happen from damage or disease in the pericardium. The excess fluid from pericardial effusion can cause intense pressure on your heart and damage it. A pericardial cyst is a noncancerous, fluid-filled growth in the pericardium. This type of cyst is very rare, affecting only 1 in , people. However, if they press on your lungs or other structures in your chest, they can cause complications like inflammation or severe bleeding.
Rarely , a pericardial cyst can lead to heart failure. Acute pericarditis starts suddenly and lasts only a few weeks.
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