Chronic constrictive pericarditis

An overview of chronic constrictive pericarditis parietal pericardium was involved and the visceral chronic inflammatory process. Caused pericardial thickening and fibrosis, diastolic heart of the restrictions on activities, thereby reducing cardiac function. Etiology of chronic constrictive pericarditis is a major cause of mycobacterial infections. Bacteriology and histological examination confirmed the change to TB 30%. About 50% of the cases were not clear risk factors. But many cases because long-term antibiotic therapy, in the case of pericardial narrow, tuberculosis evidence has disappeared. Therefore, it was felt that in most cases of tuberculosis pericarditis, followed by septic infections. Traumatic and non-traumatic pericardial blood lead constrictive pericarditis who account for about 10%. In recent years, after heart surgery with the patient increased. Pathogenesis constrictive pericarditis major pathophysiological changes due to the narrow limits of bilateral cardiac ventricular normal activities. Early illness, mainly ventricular diastolic performance for advanced cardiac diastolic be restricted, with the progress of the disease. Diastolic-have also been significantly affected. Left ventricular diastolic period, ventricular pressure increased rapidly left and right ventricular delay returning blood, venous hypertension, performance of the jugular vein engorgement, hepatomegaly, ascites, pleural effusion and generalized edema, a minority of patients, there will be splenomegaly. Cardiac output was slightly lower than normal, stroke volume decreased noticeably. In physical activity or in serious narrowing, mainly by increased heart rate per minute to maintain cardiac output. Atrioventricular groove and the vascular ring narrow root there, it may produce parts of the valve dysfunction murmur and signs. Ascites and edema around the extent of the disease is disproportionate to the one major characteristic. Ascites the mechanism has the following three points : ① resistive congestive liver, liver venous obstruction; ② diaphragm surface of pericardial adhesions affect lymphatic flow; ③ lower plasma albumin. Pathological changes generally thickened pericardium, but the extent of the inconsistency thickening, Bilateral ventricular septal surface performance and pericardial thickening more significant. Thickening of the pericardium by fibrous tissue form. The deposition of calcium plaque formation or calcification of herpes, can also form a complete bony shell. Early pericardial cavity can effusion, epicardial attachment on the thin layer of fibrous tissue or cellulose. With the progress of the disease, visceral pericardial cavity between the progressive development of the 1947 adhesion, adhesion close, and even closer integration, in the latter between the visceral pericardium no obvious interfaces. Thickening of the pericardium with the diaphragm, pleural adhesions and mediastinal structures. Early constrictive pericarditis there epicardium atrophy, late diffuse atrophy and ventricular wall thickness greater than normal thin. Also due to chronic inflammatory infiltration occurred focal myocarditis, of myocardial fibrosis. A few cases, the location of atrioventricular groove, there will be a narrow ring. In addition to heart, lung, liver, spleen and other organs can be passive decongestants and fibrosis, and long-term heart failure caused by a similar change. Half of patients with clinical onset is slow, not consciously developed symptoms of acute pericarditis no history of seizures. About 30% of patients with acute months ago pericarditis history, the symptoms were relieved after treatment has been gradually increasing. The course of patients vary in length and up to 10 years the elderly. Most patients in the event of symptoms and diagnosis, has been a year and a half to two years of history. Common symptoms of difficulty in breathing, swelling, edema, fatigue weakness and coughing. All patients exist to varying degrees of respiratory difficulties, mild physical activity that is, shortness of breath. Severe cases may sit performance to breathe. Breathing more difficult because pleural effusion or ascites due to the diaphragm with increased lung volume reduction. Although pulmonary venous pressure increased, but very few cases of interstitial lung edema. Therefore, paroxysmal nocturnal dyspnea and acute pulmonary edema relatively rare. Distension of the liver, ascites due to bad blood and offal. Renal blood flow, the body of water and sodium retention, and the surrounding edema have more performance to ankle edema. While there palpitations, fatigue weakness, and loss of appetite, abdominal discomfort, and other symptoms. In addition, coughing and heart before Dull Pain also more common. Yung was chronic patients, facial swelling, superficial vein filling, the jugular vein dilatation. Friedreich observed levy. That is, when the jugular vein pulsatility performance of the early diastolic Depression. When the narrowing of the right ventricle seriously affect efforts to flow, inspiratory observed jugular rolled obvious (Kussmaul levy). If the volume of pleural effusion, intercostal space can be widened. Half of patients apexcardiogram weaken or disappear, heart or normal spontaneous delivery sector increased slightly. Sometimes in cardiac contraction can be observed during the apex and the left sternal region was changed back down, In early diastolic rapidly outward movement. Faster heart rate. About 2 / 3 of patients to be heard early diastolic third heart sound is due to the rapid ventricular early diastolic filling induced. All patients had abdominal bulging, swelling of the liver, ascites patients. About 10% of the patients experienced splenomegaly. Normal or low blood pressure, reduced systolic blood pressure for performance. Venous hypertension, size cycle time extension. Patients often Qi network of inspiratory pulse weakened or lost. Sphygmomanometer measured inspiratory breath when systolic blood pressure lower than 10 mmHg. Some people think these changes are thickened pericardium and the diaphragm adhesion fixed together, diaphragmatic breathing down stretch pericardium, Tension increased so that the heart and restrict filling, thus decreased cardiac output, resulting in systolic blood pressure dropped.