The normal gross and microscopic structure of the human pericardium is reviewed in information. Based on the structural components of the pericardium, the pathologic responses commonly checked out in clinical specimens are presented. This offers a corfamily member explanation to clinical evolution and also diagnostic imaging findings such as delayed improvement in the workup of pericardial condition.
You are watching: Another name for the parietal pericardium is the
We existing the gross and microscopic structure of the pericardium as a framework of recommendation that have the right to be associated through present cardiac imaging methods and also interventions. The limited collection of responses of the pericardium to varied pathologic stimuli is depicted in the context of its normal framework.
A. Gross Structure of the Parietal and Visceral Pericardium
The pericardium is a roughly flask-shaped sac that consists of the heart and proximal parts of the great vessels
The pericardium is conventionally separated right into parietal and also visceral pericardium
Anterior view of the undamaged pericardial sac. An undamaged pericardium attached to the diaphragm is presented via the mediastinal pleura extending the lateral surdeals with of the pericardial sac. Note the numerous epipericardial adipose tconcern in the anterior mediastinum and also anterior cardiophrenic angles. The arrowheads flank the borders of the sternopericardial ligament. LCC = left common carotid artery. SVC = superior vena cava.
Right lateral watch of the heart and also pericardium. The ideal phrenic nerve and also pericardiophrenic vessels lie in between the parietal pericardium and also mediastinal pleura anterior to the pulmonary hilum. The arrowheads highlight these structures. Note the numerous adipose tproblem spanning the mediastinal surchallenge of the pericardium in the anterior and also lateral surfaces. RIPV = appropriate inferior pulmonary vein. RPA = best pulmonary artery. RSPV = appropriate superior pulmonary vein. SVC = Superior vena cava.
Left lateral watch of the heart and pericardium. The course of the left phrenic nerve and also steustatiushistory.orgompanying vessels are highlighted by the arrowheads. Ao = aorta. LIPV = left inferior pulmonary vein. LPA = left pulmonary artery. LSPV = left remarkable pulmonary vein.
Parietal vs. visceral pericardium. The pericardium has, as many various other serosal surfaces, a parietal and also a visceral component. The parietal pericardium is created of two layers: a serosal lining (thin red line) and a fibrous sac (thicker yellow line). The visceral pericardium or epicardium is composed of a single layer of serosal investment extending the entire heart (thin red line overlying the myocardium in blue). Note that the serosal lining of the parietal and also visceral pericardium is a continuous layer of mesothelial cells. The serosal layer of the parietal and visceral pericardium challenge each other. The potential area lined by the serosal layers is the pericardial cavity.
Parietal and also visceral pericardium. A: Coronal section of the heart reflects the ventricles, ascfinishing aorta (Ao), and partial views of the ideal and also left atrial appendages, the premium vena cava (SVC), the aortic valve, and also the pulmonary artery trunk (PA). B: The incollection of the left lateral ventricular wall is enhanced. The visceral and parietal pericardium are in close apposition and also the area between these 2 layers is virtual. The arrowheads present a space of folding of the parietal pericardium wbelow it separates from the visceral pericardium. Keep in mind the lack of subepicardial fat in the lateral left ventricle. C: Light microscopic exam mirrors a thin layer of fibrous tworry (yellow) overlying the cardiac muscle (red). The "hobnail" cells lying over the thin fibrous sheet are the mesothelial cells which create the visceral pericardium. Note the close proximity of the myocardial capillaries to the mesothelium of the visceral layer. This rich network of vessels have the right to administer quick deliver of liquid material in and also out of the pericardial area. D: A cshed up of the incollection on the ideal ventricle in 3A is presented. Tbelow is a distinctive space in between the parietal pericardium (arrowheads) and the epicardium extending the adipose tproblem that overlies the best ventricular myocardium (RV). E: Light microscopy of the mesothelial lining over the adipose tworry of the best ventricle (visceral pericardium). Short elastic fibers (black) are existing in the subepicardium. F: This micrograph of full thickness pericardial sac shows the fibrosa layer of the parietal pericardium. Note the sporadic vascularization of the fibrosa. The mesothelial cells of the parietal pericardium are directly attached to the fibrosa in the top component of the photo. The mediastinal aspect (lower part) of the pericardium shows adipose tconcern which, in turn, is likewise spanned by mesothelial cells forming the serosa of the mediastinal pleura. Ao = aorta. LV = left ventricle. PA = pulmonary artery. RV = best ventricle. SVC = exceptional vena cava. * = inferior aortic recess. ** = left pulmonic recess.
B. Pericardial Sinoffers and also Recesses
The reflections of the serosa about the good vessels entering and leaving the heart form the pericardial sinprovides and also recesses.2 The ascfinishing aorta and major pulmonary artery together are completely ensheathed by an investment of the visceral pericardium. This investment creates a potential room, the transverse sinus, which sepaprices the anteriorly located good arteries from the veins posteriorly
A second investment of visceral pericardium separately covers the venae cavae and pulmonary veins. The postcaval recess lies behind the premium vena cava and is bounded by the best pulmonary artery superiorly and ideal remarkable pulmonary vein inferiorly. The ideal and left pulmonary venous recesses are created by the pericardial reflection in between the particular superior and also inferior pulmonary veins. The cul-de-sac located behind the posterior wall of the left atrium is the oblique sinus
Sinsupplies and recesses of the pericardium. In this picture the anterior (ventral) percent of the pericardium and also the heart have actually been rerelocated to display the good vessels at the base of the heart. The aorta and pulmonary artery has actually been transected to display the course of the transverse sinus (dotted line) that sepaprices the arteries from the venae cavae and also pulmonary veins. The pericardial reflection exhas a tendency to the proximal aortic arch and also the recess between the aorta and also the premium vena cava is called the remarkable aortic recess (dotted line). The left lateral expansion of the transverse sinus is the left pulmonic recess bordered by the left pulmonary artery and left premium pulmonary vein. The oblique sinus is the cul-de-sac behind the left atrium and also bound by the pericardial reflection over the inferior pulmonary veins and also the inferior vena cava. IVC = inferior vena cava. LPA = left pulmonary artery. LPV = left pulmonary veins. RPA = ideal pulmonary artery. RPV = best pulmonary veins. SVC = premium vena cava.
C. Microscopic Organization of the Pericardium
Three unique layers can be characterized in the parietal pericardium by microscopic exam: the serosa, the fibrosa, and also an outer layer of epipericardial connective tconcern. The serosa is the innermany surface of the pericardial sac and also is formed by mesothelial cells
The visceral pericardium
A sheet of mesothelial cells is presented at high magnification. These cells deserve to differ from level to cuboidal in shape. Microvilli (arrowheads) are present on the surface dealing with the pericardial cavity to rise the surconfront area of these cells. The microvilli impart a "fuzzy" look to the luminal border of the mesothelial cells.
D. Pericardial Responses to Injury
While the fibrous tproblem bundles in the inner fibrosa via its cephalocaudal orientation perform not distend incredibly much; in comparison, the weaved company of the fibrous tworry bundles of the outside fibrosa enables for some distention of the pericardial sac prior to physiologic constriction is clinically noticeable. The specialized nature of the mesothelial cells through plentiful microvilli and also the liquid deliver devices through these cells allow for high transfer capacity via the serosal pericardium. The extremely vascularized epicardium can provide huge move of liquid to the mesothelial cells for these to produce transudays and also exudates. This defines how basic transudays and/or extremely fibrinous exudates have the right to easily form in the pericardial cavity when tright here is injury.
2. Exudative and also inflammatory response
The pericardium (parietal and visceral) has actually a restricted response to injury, which is initially materialized as increased production of pericardial liquid.4 The effusion could be a transuday which is composed largely of thin liquid or an exuday which has huge quantities of fibrin and, as a role of severity, variable numbers and also types of inflammatory cells
Fibrinous exuday. Light micrograph of the epicardial surface of the myocardium reflecting mild inflammatory infiltprice in the myocardium and also an exuberant eosinophilic fibrinous exudate on the surconfront of the visceral pericardium. The gross pathology of this fibrinous exuday is illustrated in Figure 7.
Gross specimen of a heart of a patient through uremic pericarditis completely spanned through fibrinous strands which in enhancement present yellow/green discoloration as the patient had jaundice. Keep in mind that the fibrin strands surround the root of the good vessels as these segments are intrapericardial. Ao = aortic valve and aortic root. LV = left ventricle. PA = pulmonary artery and valve. RV = ideal ventricle. RVOT = right ventricular outcirculation tract. SVC = premium vena cava.
Coronal area of the heart mirroring organized fibrous (not fibrinous) strands (asterisk) formed in between the visceral pericardium and the parietal pericardium. Keep in mind that the parietal pericardium is slightly thicker than the normal examples in Figure 3. LA = left atrium. LAA = left atrial appendage. LLL = left lower lobe of the lung. PA = pulmonary artery at bifurcation.
3. Reabsorption, company and repair of the exudative inflammatory response
The healing process may show a number of alternate preleading fads as displayed in Figure 9. These responses have the right to be of a single form or merged processes
Usual responses of the pericardium to noxious stimuli cause varied non-exclusive kinds of effusions. A serous effusion may take place and be reabsorbed entirely without leaving any kind of histologic modification. On the various other hand also, exudative effusions always leave a trace of the pericardial response to the injury. The exuday of fibrin is the a lot of common finding regardmuch less of the resource of injury: chemical (uremic, pharmaceuticals), physical (open heart surgery, therapeutic ablation, radiation), or contagious (viral, bacterial, fungal, parasitic). Once the fibrinous or fibrino-hemorrhagic exudate occurs, there is usually an inflammatory response elicited that will certainly "clean" the fibrinous debris. During this phase, the inflammatory cells promote the development of neovascularization and also early on extracellular matrix deplace (granulation tissue). If the noxious stimulus ends, the result is commonly mild fibrosis. If the noxious stimulus persists, the response of the pericardium is extended in regards to the process of exudation, inflammation, and also repair. In recurrent pericarditis, the inflammatory response may wax and also wane. The red arrows illustrate points where a reexisting insult deserve to happen aacquire, hence editing and also lengthening the healing process. The repetitive injury-repair cycles lead to thickening of the parietal pericardium and also adhesion to the visceral pericardium through obliteration of the pericardial cavity. While generally checked out, calcification is not always a feature present during the healing of the pericardium.
Acute fibrinous pericarditis. A and also B: Fibrinous exudates via abundant inflammatory cells are presented. The fibrosa layer mirrors dilated vessels. The incollection mirrors a cshed up of the inflammatory infiltprices intermingled via the fibrinous strands and also reenergetic mesothelial cells in the serosa layer of the parietal pericardium. C and also D: Parietal pericardium through abundant inflammatory infiltrates and also beforehand deplace of extracellular matrix (yellow green color in D on optimal and listed below the fibrosa). This is a very early phase of organization of the exudate. The newly created connective tissue eventually is got into by capillaries that form extensive vascular network-related. The fibrosa layer of the parietal pericardium is delineated by the dotted lines. Note that in this example the inflammatory procedure is including both the pericardial serosa (mesothelial) layer and also the mediastinal pleural serosa layer. If a pericardiectomy is perdeveloped, the inflammation existing in the mediastinal pleura might still current clinically as residual "pericardial" referred pain. (A and C: H&E stain. B and D: Movat pentachrome stain).
If no further injurious stimuli are present, the inflammatory cells within the fibrinous exudate promote neovascularization and also fibroblast proliferation. Extracellular matrix is laid dvery own and as it matures, the loose granulation tworry becomes organized via even more mature fibrous tproblem while the neovascularization and also chronic inflammation end up being less conspicuous
Organizing pericarditis via conspicuous neovascularization. Note that the fibrosa layer does not have actually extremely conspicuous vessels compared to the area of arranging fibrosis. (H&E stain and also Movat pentachrome stain).
The fibrous proliferation of the pericardium might mostly involve only among the serosal components or might involve both the parietal and also visceral pericardium. If repeated episodes of pericarditis happen (regardmuch less of the etiology), the response of the pericardium is comparable in developing new acute fibrinous and/or fibrino-hemorrhagic exudays which cause new granulation tproblem and even more neovascularization
Maturing arranging pericarditis. Loose edematous granulation tworry becomes arranged right into denser, thicker fibrous tconcern as the amount of extracellular matrix and inflammation diminishes. Relative abundance of fibroblasts (fibroplasia) and also newly-formed blood vessels are indications of the task of the process. Compare to Figure 13. (H&E stain and also Movat pentachrome stain).
Organized pericarditis through represent insult. These micrographs display dense, mature bundles of fibrous tconcern overlying the fibrosa layer of the pericardium. The neovascularization is much less conspicuous than in the earlier stages of organization (Figures 11 and also 12). In this instance, tbelow is boosted cellularity in the top strata of the pericardium in the direction of the pericardial cavity. This innermost area in the direction of the pericardial cavity shows plentiful fibroblast proliferation or fibroplasia, displayed as dark blue infiltrates in upper left area of the imperiods. In enhancement, tbelow is also fibrin and hemorrhage. This is a typical example of a represent process. (H&E stain and also Movat pentachrome stain).
Dense fibrous pericarditis without calcification. The parietal pericardium is thickened as a result of the additional dense (yellow) fibrous tproblem that mirrors no fibroblasts, inflammatory infiltprices or neovascularization. This represents a quiescent phase however may currently be linked via pericardial constriction. (H&E stain and Movat pentachrome stain).
If the cause of the pericardial effusion is main or metastatic malignant neoplasm, the malignant cells have the right to be readily watched in the time of microscopic examination
Metastatic lung adenocarcinoma. An organizing fibrinous exuday containing metastatic tumor cells is present. Mild inflammatory infiltrate is detailed in the fibrosa layer of the parietal pericardium. The inset shows a cluster of metastatic tumor cells with large pleomorphic nuclei in a channel lined by level endothelial cells. (H&E stain and Movat pentachrome stain).
See more: How And Why Did Ash Lose The Kalos League Finals Against Alain : Pokemon
ReferencesFerrans VJ IT, Roberts WC. Anatomy of the pericardium. In: Reddy PS LD, Shaver JA, eds. Pericardial Disease. New York: Raven Press; 1982:15-29.Levy-Ravetch M, Auh YH, Rubenstein WA, Whalen JP, Kazam E. CT of the pericardial recesses. AJR Am J Roentgenol 1985;144:707-14.Ishihara T, Ferrans VJ, Jones M, Boyce SW, Kawanami O, Roberts WC. Histologic and ultrastructural functions of normal human parietal pericardium. Am J Cardiol 1980;46:744-53.Klein AL, Abbara S, Agler DA, et al. Amerihave the right to Society of Echocardiography clinical references for multimodality cardiovascular imaging of patients via pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and also Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr 2013;26:965-1012.
Clinical Topics: Cardiac Surgery, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Pericardial Disease, Vascular Medicine, Aortic Surgery, Interventions and Imaging, Interventions and Vascular Medicine
Keywords: Pericardium, Adenocarcinoma, Adipose Tissue, Aorta, Thoracic, Aortic Valve, Cardiac Imaging Techniques, Carotid Artery Thrombosis, Cicatrix, Coloring Agents, Constriction, Endothelial Cells, Epithelial Cells, Extracellular Matrix, Fibrinolysis, Heart Ventricles, Inflammation, Mast Cells, Microvilli, Myocardium, Pericardial Effusion, Pericardiectomy, Pericarditis, Constrictive, Phrenic Nerve, Pulmonary Artery, Pulmonary Veins, Sagittaria, Vena Cava, Inferior, Vena Cava, Superior
YOU ARE HERE: Home > Latest in Cardiology >Structure of the Person Pericardium and Responses to Pathologic Processes
Jsteustatiushistory.org Journals on steustatiushistory.org
Latest in Cardiology
Education and also Meetings
Tools and Practice Support
Heart Housage 2400 N Street NW Washington, DC 20037 Phone: (800) 253-4636, ext. 5603 or (202) 375-6000, ext. 5603 E-mail: membercare