The serous pericardium, the inner layer of the pericardium, is composed of two different layers. The outer layer, the parietal layer , is completely adhered to the fibrous pericardium. The inner layer is known as the visceral layer , which covers and protects the great vessels and heart.
The space between the parietal and visceral layers is called the pericardial cavity. The visceral layer is referred to as the epicardium in the areas where it is in direct contact with the heart. The space between these two serous layers, the parietal and the visceral, is the pericardial cavity, which contains pericardial fluid. The serous pericardium, with its two membranes and the fluid-filled pericardial cavity, provides protection to the heart and a lubricated sliding surface within which the heart can move in response to its own contractions and to the movement of adjacent structures such as the diaphragm and the lungs.
The pericardium is important because it protects the heart from trauma, shock, stress, and even infections from the nearby lungs. The pericardium lubricates the heart and prevents it from becoming too large if blood volume is overloaded though it will not prevent chronic heart enlargement.
Despite these functions, the pericardium is still vulnerable to problems of its own. Pericarditis is the term for inflammation in the pericardium, typically due to infection. Pericarditis is often a severe disease because it can constrict and apply pressure on the heart and work against its normal function.
Pericarditis comes in many types depending on which tissue layer is infected. The heart wall is comprised of three layers: the outer epicardium, the middle myocardium, and the inner endocardium.
The heart wall is comprised of three layers, the epicardium outer , myocardium middle , and endocardium inner. These tissue layers are highly specialized and perform different functions. During ventricular contraction, the wave of depolarization from the SA and AV nodes moves from within the endocardial wall through the myocardial layer to the epicardial surface of the heart.
The Heart Wall : The wall of the heart is composed of three layers, the thin outer epicardium, the thick middle myocardium, and the very thin inner endocardium. The dark area on the heart wall is scarring from a previous myocardial infarction heart attack.
The outer layer of the heart wall is the epicardium. The epicardium refers to both the outer layer of the heart and the inner layer of the serous visceral pericardium, which is attached to the outer wall of the heart. The epicardium is a thin layer of elastic connective tissue and fat that serves as an additional layer of protection from trauma or friction for the heart under the pericardium. This layer contains the coronary blood vessels, which oxygenate the tissues of the heart with a blood supply from the coronary arteries.
The middle layer of the heart wall is the myocardium—the muscle tissue of the heart and the thickest layer of the heart wall. It is composed of cardiac muscle cells, or cardiomyocytes. Cardiomyocytes are specialized muscle cells that contract like other muscle cells, but differ in shape. Compared to skeletal muscle cells, cardiac muscle cells are shorter and have fewer nuclei. Cardiac muscle tissue is also striated forming protein bands and contains tubules and gap junctions, unlike skeletal muscle tissue.
Due to their continuous rhythmic contraction, cardiomyocytes require a dedicated blood supply to deliver oxygen and nutrients and remove waste products such as carbon dioxide from the cardiac muscle tissue. This blood supply is provided by the coronary arteries. The inner layer of the heart wall is the endocardium, composed of endothelial cells that provide a smooth, elastic, non-adherent surface for blood collection and pumping.
The endocardium may regulate metabolic waste removal from heart tissues and act as a barrier between the blood and the heart muscle, thus controlling the composition of the extracellular fluid in which the cardiomyocytes bathe. This in turn can affect the contractility of the heart.
This tissue also covers the valves of the heart and is histologically continuous with the vascular endothelium of the major blood vessels entering and leaving the heart. The Purkinje fibers are located just beneath the endocardium and send nervous impulses from the SA and AV nodes outside of the heart into the myocardial tissues. The endocardium can become infected, a serious inflammatory condition called infective endocarditis.
This and other potential problems with the endocardium may damage the valves and impair the normal flow of blood through the heart. The heart has four chambers. The two atria receive blood into the heart and the two ventricles pump blood into circulation.
The heart is the complex pump of the circulatory system, pumping blood throughout the body for the purposes of tissue oxygenation and gas exchange. The heart has four chambers through which blood flows: two sets of each type of chamber atria and ventricles , one per side, each with distinct functions.
The left side of the heart deals with systemic circulation while the right side of the heart deals with pulmonary circulation. The atria are chambers in which blood enters the heart. They are located on the anterior end of the heart, with one atrium on each side.
The right atrium receives deoxygenated blood from systemic circulation through the superior vena cava and inferior venae cavae. The left atrium receives oxygenated blood from pulmonary circulation through the left and right pulmonary veins. Blood passively flows into the atria without passing through valves.
The atria relax and dilate expand while they fill with blood in a process called atrial diastole. The atria and ventricles are separated by the mitral and tricuspid valves.
The atria undergo atrial systole, a brief contraction of the atria that ejects blood from the atria through the valves and into the ventricles. The chordae tendinae are elastic tendons that attach to the valve from the ventricles and relax during atrial systole and ventricular diastole, but contract and close off the valve during ventricular systole. One of the defining characteristics of the atria is that they do not impede venous flow into the heart.
Atria have four essential characteristics that cause them to promote continuous venous flow:. The ventricles are located on the posterior end of the heart beneath their corresponding atrium. The right ventricle receives deoxygenated blood from the right atria and pumps it through the pulmonary vein and into pulmonary circulation, which goes into the lungs for gas exchange. The left ventricle receives oxygenated blood from the left atria and pumps it through the aorta into systemic circulation to supply the tissues of the body with oxygen.
The walls of the ventricles are thicker and stronger than those of the atria. The physiologic load on the ventricles, which pump blood throughout the body and lungs, is much greater than the pressure generated by the atria to fill the ventricles. Further, the left ventricle has thicker walls than the right because it pumps blood throughout the body, while the right ventricle pumps only to the lungs, which is a much smaller volume of blood.
During ventricular diastole, the ventricles relax and fill with blood. During ventricular systole, the ventricles contract, pumping blood through the semi-lunar valves into systemic circulation.
Structure of the heart : Structure diagram of a coronal section of the human heart from an anterior view. The two larger chambers are the ventricles. The human circulatory system is a double system, meaning there are two separate systems of blood flow: pulmonary circulation and systemic circulation. The inferior lobe is a section of the human lung. Each lung is divided into lobes; the right lung consists of the superior, middle, and inferior lobes,.
The pulmonary trunk is a major vessel of the human heart that originates from the right ventricle. It branches into the right and left pulmonary…. Within the body, there are a total of four pulmonary veins, and all of them connect to the left atrium of the heart.
The heart pumps oxygen-depleted…. The main pulmonary artery is responsible for transporting oxygen-depleted blood away from the heart and back toward the lungs. The main artery splits…. The vagus nerve is the longest of the 12 cranial nerves. It is therefore reasonable that any reason that elevates pressure of the left atrium has the potential to increase the pulmonary venous pressure, because of the higher impedance of draining blood forward and larger regurgitated volume from the high-pressured left atrium.
Another important characteristic of vessel that we cannot forget when we are discussing the hemodynamic is the vascular distensibility and compliance.
Distensibility is an ability of vessel whose volume can increase or decrease for every increase or decrease intravascular pressure, and the compliance is equal to distensibility times the volume of blood in the given portion of the circulation. Because of the different wall constitution between veins and arteries, the distensibility of veins is about eight times larger than that of arteries.
That is, the venous system can conserve more blood and only has slightly elevation of the intravascular pressure [ 15 ]. The pulmonary veins have similar distensibility to the systemic veins, meaning that the pulmonary venous pressure would not exceed the normal range before large amount of blood is congested in the pulmonary capillary and veins. Various congenital and acquired cardiovascular diseases that affecting pulmonary veins themselves and the left atrium could lead to the congestion of pulmonary veins.
They can be simply classified into conditions that cause obstruction or pulmonary overcirculation. Occlusions of one or more pulmonary veins, and the divided left atrium like the CTS are examples that pulmonary venous blood flow has difficulties to get through obstacles in its normal pathway and therefore causing high pressure to the rest part of pulmonary veins.
In addition, pulmonary overcirculation caused by intra- or extra-cardiac left to right shunting atrial and ventricular septal defects, patent foramen ovale, patent ductus arteriosus, and anomalous pulmonary venous connection and so on also has the potential to causes pulmonary congestion because of larger than normal volume that circulates the pulmonary vasculature.
We will discuss these diseases in the following sections. The CTS is a relatively rare congenital cardiovascular disease that has been first reported in [ 16 ].
In an autopsy research, it was accounted for 0. In veterinary medicine, the true prevalence is hard to know because this abnormality is not always producing heart murmur and develops clinical signs that can be observed by the owner and the veterinarian at the general practice.
By reviewing case reports, naturally-occurred CTS is identified more frequently in cats [ 18 , 19 , 20 , 21 , 22 , 23 ] than in dogs [ 24 , 25 , 26 ].
The embryonic cause of CTS is still controversial, but the theory of pulmonary venous abnormality is the most popular. In the development of pulmonary veins, they should incorporate with left atrium and form four ostia on the smooth part of the dorsal left atrial wall.
If certain degree of failure in this process occurs, the left atrium could be separated by the remains of the pulmonary veins, most of the time is a fibromuscular membrane.
The left atrium is therefore divided to a proximal chamber that locates between the atriopulmonary junction and the fibromuscular membrane, and a distal chamber that extends from the fibromuscular membrane to the mitral valve annulus. The molecular cause of CTS was first reported in experimental mice without hyaluronidase 2, which is an enzyme required for the degradation of hyaluronan that is the major extracellular matrix component of the heart [ 27 ]. Later, the similar result was obtained by genetic studies in affected human families and mice [ 28 ].
Anatomic variation of the membrane exists and whether or how much of the blood flow would be impeded depends on the three-dimensional relative position between the membrane and left atrium.
This intra-atrial septum can be complete, incomplete or fenestrated, and its size, shape, thickness and location can be varied among affected patients.
Types of diaphragmatic, hourglass and tubular has been used to describe the variations [ 29 ]. In a retrospective study, the histopathology of the membranous tissue was investigated. Elastin fibers were found to be presence in the top and bottom side and was absent in the middle layer of the diaphragm. Cardiomyocytes with positive staining of cardiac troponin C were located in the peripheral region, more on the side that near the diaphragm and atrial septum than on the side that near the diaphragm and the atrial free wall.
The remanent area was mostly made up by the fibrous collagen and other mesenchymal cells. These specimens were collected from human patients that undergo surgical repair of the Cor triatriatum sinister, without surgical death in this cohort [ 30 ]. Impendence of the blood flow in the left atrium could cause turbulence, but the pressure gradient between two chambers may be not large enough for the heart murmur to be heard.
Elevated pressure in the proximal chamber of the left atrium could raise the intravascular pressure of the pulmonary veins, and signs of left-side congestive heart failure may occur. However, the natural progression of the CTS in human patients is generally stable, with more than half patients were diagnosed in adulthood. In patients that need surgical correction using cardiopulmonary bypass, the surgery is safe and effective [ 31 ].
Transthoracic echocardiography is usually helpful in making diagnosis [ 32 ]. Except for detecting Cor triatriatum sinister, the echocardiography can also identify concurrent lesions. Two feline cases had been published that one kitten had CTS combined with persistent left cranial vena cava [ 20 ], and the other was diagnosed CTS with incomplete atrioventricular septal defect [ 21 ].
Some conditions can mimic the CTS under two-dimensional imaging mode, including supramitral ring or pulmonary stenosis [ 34 ].
In cases that the echocardiographic result alone is controversial or is suspicious of having multiple cardiovascular developmental diseases, additional imaging tools should be considered. In some conditions especially when our target area is located near the heart base, the transesophageal echocardiography can provide better image resolution and details than the transthoracic echocardiography.
Cardiac catheterization angiography has its advantages that it can measure the true intra-lumen pressure, which is always an estimated value if only echocardiography is performed. However, its clinical utility is limited in the veterinary field because deep sedation to generalized anesthesia is usually required in veterinary patients. Other imaging tools like computed tomography angiography and magnetic resonance imaging can provide multiplaner image reconstruction and assist with the diagnosis process [ 29 ].
Early in the , a kitten presented signs of respiratory distress and diagnosed with CTS was successfully surgically managed. The membrane was torn by a dilator introduced from an opened left atrium [ 18 ]. However, if the opening is small and restrictive, it can be surgically repaired. Pulmonary Arteriovenous Malformation.
This is a condition in which there is communication between the pulmonary artery and pulmonary vein. It may be asymptomatic or cause shortness of breath. After birth and in adults, the pulmonary veins may be affected by narrowing or obstruction, increased pressure, and blood clots thrombosis.
Pulmonary Vein Stenosis. Stenosis or narrowing can occur in the pulmonary veins, similar to narrowing in arteries such as the coronary arteries.
When narrowed, angioplasty may be done or stents placed to maintain the caliber of the vein. Pulmonary vein stenosis sometimes occurs after ablation for atrial fibrillation. Pulmonary Vein Obstruction. The pulmonary veins may become obstructed in a few conditions, such as lung cancer or tuberculosis. Worsening shortness of breath in someone with lung cancer can be a sign of this complication.
Surgical and Procedural Damage. The pulmonary veins may also be damaged during surgical procedures. This includes the different types of surgery for lung cancer.
Radiofrequency ablation for arrhythmias may also result in damage. Pulmonary Venous Hypertension. Pulmonary hypertension is a condition in which the pressure in the pulmonary veins is elevated. It occurs most commonly with left heart failure, as blood backs up into the veins due to inefficient contractions of the heart. Several other types of heart disease can lead to pulmonary venous hypertension as well, including conditions such as mitral stenosis.
Symptoms can include shortness of breath, swelling of the legs, and fatigue. It is diagnosed with a right heart angiogram, which finds an increase in capillary wedge pressure. The primary treatment is to address the underlying cause of the disease. Pulmonary Vein Thrombosis. Blood clots may form in the pulmonary vein as with other blood vessels but are quite uncommon. When it does occur, it is often related to a malignancy such as lung cancer.
Role in Atrial Fibrillation. The science connecting the pulmonary veins with atrial fibrillation is relatively new. It's thought that the thin layer of myocardial tissue that covers the pulmonary veins can be the focus of atrial fibrillation, with some regions and veins playing a larger role than others. Pulmonary vein isolation is a procedure that is sometimes done to treat atrial fibrillation. In this procedure, scar tissue is created in the left atrium where each of the four pulmonary enters, which can sometimes control the arrhythmia when other treatments such as medications fail.
A complication that sometimes occurs with this procedure is pulmonary venous stenosis discussed above. Sign up for our Health Tip of the Day newsletter, and receive daily tips that will help you live your healthiest life.
Normal distal pulmonary vein anatomy. Marty M, Lui F. Embryology, fetal circulation. In: StatPearls. Updated January 14, Boyette LC, Burns B. Physiology, pulmonary circulation. Updated April 3, Tucker WD, Mahajan K.
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