Chronic pericarditis

Overview of acute pericarditis, pericardial the scar left on adhesion and calcinosis. Most patients only minor scar formation and osteoporosis or partial adhesion, no obvious pericardial thickening not affect cardiac function, known as chronic adhesive pericarditis (chronic adhesive pericarditis), no clinical importance. Some patients with chronic pericardial effusion, chronic exudative pericarditis (chronic effusive pericarditis), may be non-specific acute pericarditis chronic process, mainly for the performance of pericardial effusion, and the prognosis is good. a few patients due to the formation of scar tissue removed, pericardial lost scalability, significant effects on the heart systolic and diastolic function, called constrictive pericarditis. It includes the typical chronic constrictive pericarditis (chronic constrictive perica rditis), and pericardial effusion in the same time has narrowed the pericardial fluid nature of subacute constrictive pericarditis (sub acute effusive constrictive pericarditis), in the latter, there are clinical pericardial plug pericardial have narrowed the performance and eventually evolved into a typical chronic constrictive pericarditis. This section discussed chronic constrictive pericarditis in a series of clinical problems. Etiology constrictive pericarditis secondary to acute pericarditis, sometimes clinically observed acute changes to narrow the development process, However, the majority of cases of acute phase symptoms not obvious, constrictive pericarditis to the performance obviously has often lose the pathological features of the disease, Many patients therefore causes not sure. Certainly in the etiology of tuberculous pericarditis accounted for the majority of non-specific pericarditis Secondly, Radiation therapy and open heart surgery in gradually increased, and a few of purulent pericarditis and traumatic pericarditis. Rheumatic pericarditis caused cardiac little narrow. Occasionally, rheumatoid arthritis, systemic lupus erythematosus, uremia, Histoplasma Capsulatum disease, tularaemia disease, actinomycosis. Coxsackie B virus infection, influenza, infectious mononucleosis syndrome, herpes simplex, Salmonella disease, spine coccidiosis, schistosomiasis, amoebic diseases, malignant tumors, pericardial foreign body, chylothorax pericarditis, cholesterol pericarditis, dialysis treatment, kidney transplants and anticoagulant therapy after pericardial blood lead constrictive pericarditis report. As technology improved diagnosis, inflammation can be found in some of (the virus, with primary mediastinal fibrosis, or sarcoidosis), uremia, New biological and trauma (including heart surgery and radiotherapy) of constrictive pericarditis associated with pericardial effusion, subacute form exudative constrictive pericarditis. Pathological changes in chronic constrictive pericarditis, pericardial dirty outer layer and extensive adhesions thickening and calcification. pericardial cavity occlusion become a scar tissue fiber shell, wrap tightly and oppression throughout the heart and great vessels roots, can be confined to the heart of certain parts of the surface, such as the atrioventricular groove or aortic root formation narrow ring. Especially in the ventricular surface of the right ventricle, and scars are often more sophisticated, often 0.2-2cm thick or more. In most patients, scar tissue by dense collagen fibers, and was spot or flake glass degeneration, therefore unable to find prompt primary lesions characteristic changes. Some patients were found viable within the pericardial tuberculosis or purulent of granulation tissue. As often found outside fiber layer parcels, for the enrichment of blood and body fluid composition of the regional presence, Pericardial haemorrhage suggested forming pericardium is narrowing the important factors. Normal heart shape or smaller, pericardial disease often involving close to the lower myocardial. Coarctation of pericardial activities affecting the heart and metabolism, and sometimes leads to cardiac atrophy, fibrosis, fatty infiltration and calcification. Clinical manifestations of constrictive pericarditis onset often hidden passage. Pericardial narrow the manifestations of acute pericarditis in a few months to several decades, generally 2 ~ 4 years. In narrowing the development of the early signs of symptoms often than significant, even in the late There has been a marked cycle dysfunction in patients may only minor symptoms. (1) fatigue symptoms after breathing difficulties often constrictive pericarditis most of the early symptoms, is due to cardiac output relatively fixed, the activities could not be increased. Be late because of large pleural effusions, ascites phrenic elevation and pulmonary congestion, resulting in the break occurred breathing difficulties. even sit up straight to breathe. Massive ascites and swelling of the liver oppression abdominal viscera, have abdominal swelling flu. It may be weak, Be selective receded, dizziness, weakness, palpitations, cough, abdominal pain, swelling, etc.. (2) signs of an. The performance of the heart itself hearts voiced sector normal or slightly increased. Apexcardiogram weakened or disappeared, heart sounds can be felt far and cardiac performance of these activities being restricted and cardiac output decrease. 2nd heart of a pulmonary valve components can be enhanced. Some patients in the left margin sternum third intercostal ~ 4 can be heard in a second heart sound after about 0.1 seconds of the extra early diastolic sound (pericardial tapping sound), the nature and acute pericarditis with cardiac tamponade when similar. Often faster heart rate. Sinus rhythm is normal, there may be premature beat, atrial fibrillation, atrial flutter, such as ectopic rhythm. 2. Cardiac compression performance jugular vein engorgement, hepatomegaly, ascites and pleural effusion, lower extremity edema. These diastolic disruption, reduced cardiac output, leading to the kidney of water and sodium retention, thus increasing blood volume, and venous obstruction so that the venous hypertension. Constrictive pericarditis ascites than subcutaneous edema there early, which is more substantial, and the general failure, reasons not yet clear, the following factors may be relevant; ① venous pressure and slow to sexual continues to rise so that small subcutaneous and visceral arterial spasm small artery spasm is not; ② pericardial adhesions were under the pericardial to hepatic vein into the inferior vena cava Department near the most significant, serious hepatic venous congestion. abdominal lymphatic flow significantly hampered, edema fluid in the abdominal cavity easily retention; ③ renal blood flow decreased less, water and sodium retention light, it later emerged subcutaneous edema and lighter, which is mainly distributed in the lower extremities and the lower back. Moreover, in the pathogenesis of pleural fluid can occur sooner or later. Sometimes he vein. Cardiac output decline to lower systolic blood pressure, venous congestion, the reflex surrounding small artery spasm enable higher diastolic blood pressure, Therefore pulse pressure change.