Pericarditis is the inflammation of the pericardium, often with fluid accumulation. Pericarditis can be caused by many diseases (eg. As infection, myocardial infarction, trauma, tumors, metabolic diseases), but is often idiopathic. Symptoms include chest pain or tightness, which are often worsened by deep inspiration. Cardiac output may be greatly reduced when a cardiac tamponade or constrictive pericarditis develops. The diagnosis is made due to the symptoms of a rubbing noise, ECG changes and the detection of pericardial effusion in x-ray absorption or echocardiography. Identifying the cause requires further investigation. The specific treatment depends on the cause, general measures include analgesia, anti-inflammatory drugs, colchicine and rarely surgery.

Pericarditis is the most common disease of the pericardium. Congenital Perikardkrankheiten are rare.

Pericarditis is the inflammation of the pericardium, often with fluid accumulation. Pericarditis can be caused by many diseases (eg. As infection, myocardial infarction, trauma, tumors, metabolic diseases), but is often idiopathic. Symptoms include chest pain or tightness, which are often worsened by deep inspiration. Cardiac output may be greatly reduced when a cardiac tamponade or constrictive pericarditis develops. The diagnosis is made due to the symptoms of a rubbing noise, ECG changes and the detection of pericardial effusion in x-ray absorption or echocardiography. Identifying the cause requires further investigation. The specific treatment depends on the cause, general measures include analgesia, anti-inflammatory drugs, colchicine and rarely surgery. Pericarditis is the most common disease of the pericardium. Congenital Perikardkrankheiten are rare. Anatomy The pericardium consists of two layers. The visceral pericardium is a single layer of mesothelial cells, which adhere to the myocardium, to fold back on itself about the origins of the large vessels and is combined with a tight fibrous layer to enclose the heart as a parietal pericardium. The bag formed by these two layers contains small amounts of liquid (<25-50 mL), which mainly consist of Plasmaultrafiltrat. The pericardium limits the expansion of the heart chambers and increases the efficiency of the heart. The pericardium is rich innervated with sympathetic and somatic afferents. Strain Sensitive mechanoreceptors receive changes in heart volume and wall tension and may be responsible for mediating the pericardial pain. The Nn. phrenic embedded in the parietal pericardium and easily damaged during surgery at the pericardium. Pathophysiology pericarditis can be acute subacute or chronic. Acute pericarditis develops quickly and causes an inflammation of the pericardium and often a pericardial effusion. The inflammation can expand (myopericarditis) to the epicardial myocardium. Severe hemodynamic effects or arrhythmias are rare, although a pericardial tamponade is possible. An acute disease may be subacute or chronic. These forms evolve more slowly; whose outstanding feature is effusion. Subacute pericarditis occurs within weeks to months after the triggering event on. Chronic pericarditis is defined as> 6 months persistent pericarditis. The pericardial effusion is the accumulation of fluid in the pericardium. The liquid can (sometimes with fibrin) to be sero-bleeding, bloody, purulent or chylous serous. A cardiac tamponade occurs when a large pericardial effusion impairs cardiac filling and leads to a low cardiac output and sometimes shock and death. When the liquid (usually blood) accumulates rapidly, even small amounts (eg., 150 ml) can already lead to tamponade because the pericardium can not expand quickly enough to to adapt. A slow increase to over 1500 ml does not have to lead to tamponade. A limited pericardial effusion may lead to localized tamponade of the right or left ventricle. Occasionally, the pericarditis leads to a considerable thickening and stiffening of the pericardium (constrictive pericarditis). Constrictive pericarditis, which is rare, is the result of significant inflammatory and fibrotic thickening of the pericardium. Sometimes the visceral and parietal layer adhere to each other or the myocardium. The fibrotic tissue contains calcium deposits. The rigid, thickened pericardium affects the ventricular significantly and leads to a decrease of the ejection volume and cardiac output (CO). A significant accumulation of pericardial fluid is rare. Arrhythmias are common. The diastolic pressures in the ventricles, the atria and the large venous vessels are virtually the same. Systemic venous congestion occurs, which leads to a considerable transudation of fluid from the systemic capillaries; characterized edema produced in the hanging parts of the body, followed by a later ascites. A chronic increase in the systemic venous pressure, and the hepatic venous pressure can lead to scarring of the liver, which is referred to as cardiac cirrhosis. In this case, the patient may first present to evaluate the liver cirrhosis. A narrowing of the left atrium, the left ventricle, or both, increases the pulmonary venous pressure. Occasionally a pleural effusion develops. Chronic constrictive pericarditis is less common than in the past. Subacute constriction (weeks to months after a triggering injury) is increasingly widely recognized. The transient constrictive pericarditis variant of returns spontaneously or after medical treatment. Etiology Acute pericarditis can occur as a result of an infection, an autoimmune or inflammatory disease, uremia, trauma, myocardial infarction, cancer, radiation therapy or because of certain drugs (see table: causes of acute pericarditis). The infectious pericarditis is often viral related or idiopathic. Purulent bacterial pericarditis is not common, but can of infective endocarditis, pneumonia, septicemia, a penetrating trauma or cardiac surgery follow. Often the cause can not be identified (referred to as non-specific or idiopathic pericarditis), but many of these cases are probably viral cause. Acute myocardial infarction caused 10-15% of cases of acute pericarditis. The Postmyokardinfarktsyndrom (Dressler’s syndrome) is a less common cause when the reperfusion with percutaneous transluminal coronary angioplasty (PTCA) or thrombolysis in patients with transmural infarction is not effective. Pericarditis arises (also called Postkardiotomiesyndrom) 5-30% of cardiac surgery after a pericardiotomy. Postperikardektomiesyndrom, Postmyokardinfarktsyndrom and traumatic pericarditis put the post cardiac injury syndrome are causes of acute pericarditis Idiopathic viral infections (Echo virus, influenza virus, coxsackie B virus, HIV *) Bacterial infections † (streptococci, staphylococci, gram-negative bacilli. TB †; (in children, Haemophilus influenzae) fungal infections histoplasmosis, coccidioidomycosis, blastomycosis) Parasitic infections (toxoplasmosis, amebiasis, hydatid disease) autoimmune diseases (RA, SLE, systemic sclerosis) cancer (eg. As leukemia, breast or lung cancer, and, in people with AIDS, Kaposi’s sarcoma) Radiotherapy Inflammatory diseases (amyloidosis, inflammatory bowel disease, sarcoidosis) uremia injury myocardial infarction Postmyokardinfarkt- (DRESSLER) syndrome Postperikardiotomiesyndrom Medications (eg. . B. hydralazine, isoniazid, methysergide, phenytoin, procainamide) * When patients with AIDS (lymphoma, Kaposi’s sarcoma, or certain infections such as Mycobacterium avium, M. tuberculosis, Nocardia or infections, other fungal or viral infections) develop, this may have pericarditis result. † In the US, tuberculous pericarditis makes <5% of cases of acute or sub-acute pericarditis out in some areas of India and Africa, however, the majority of cases. Subacute pericarditis is an extension of acute pericarditis and thus has the same causes. For example, occurs in some patients days or weeks after recovery from acute pericarditis, transient constriction. A chronic pericardial effusion or chronic constrictive pericarditis may follow almost etiology of acute pericarditis. Additionally, you experience some cases on without prior acute pericarditis. Hypothyroidism cause pericardial effusion and a cholesterol pericarditis. The Cholesterol pericarditis is a rare disease that is associated with myxedema and in which a chronic pericardial effusion has a high cholesterol levels, which can cause inflammation and pericarditis. Chronic pericarditis with large effusion (serous, sero-bloody or bloody) is most commonly caused by metastases, usually due to lung or breast cancer, sarcoma, melanoma, leukemia, or lymphoma. Sometimes no cause of chronic pericarditis can be detected. Transient constrictive pericarditis is most commonly caused by an infection or Postperikardiotomie or idiopathic. Fibrosis of the pericardium can accompany a purulent or pericarditis connective tissue disease. In elderly patients, malignant tumors, myocardial infarction and tuberculosis are common causes. A haemopericardium (accumulation of blood in the pericardium) can lead to pericarditis or Perikardfibrose; common causes include a chest trauma, iatrogenic injury (z. B. for cardiac catheterization, in pacemaker implantation or when placed central venous catheter) and the rupture of a thoracic aortic aneurysm. Symptoms and complaints Some patients present with symptoms and signs of inflammation before (acute pericarditis), others with symptoms and signs of fluid accumulation (pericardial effusion). The Symptoms vary depending on the severity of inflammation and the amount and rate of fluid accumulation. Even large amounts of pericardial fluid may be asymptomatic if they develop slowly (z. B. for months). Acute pericarditis Acute pericarditis tends to cause chest pain and pericardial rub, sometimes dyspnea. The first indication may be only the cardiac tamponade with hypotension, shock, or pulmonary edema. Since the innervation of the pericardium and the myocardium is the same, the chest pain at a pericarditis is sometimes similar to a Myokardentzündung or ischemia: a dull or sharp precordial or substernal pain may radiate to the neck, in the Trapeziusloge (especially the left) or the shoulders , The pain may have a mild to severe expression. In contrast to ischemic chest pain of pain due to a pericarditis usually carried movement, cough, breathing or swallowing of food is amplified and it can be improved by seating and leaning forward. Tachypnea and a non-productive cough may be present; Fever, chills and fatigue are common. At 15 to 25% of patients with idiopathic pericarditis, symptoms (recurrent pericarditis) repeat temporarily after months or years. The most important finding in the physical examination is the tThe triphasic or systolic and diastolic pericardial friction rub. However, the friction rub is often only temporary or volatile; it can only be present during systole and less frequently even during diastole. If there is no friction sound can be heard at a sitting, crouched patients who may auscultation is by listening with a stethoscope while the patient on all fours, are attempted. Sometimes during breathing a component of pleural friction noise is detected, the wird.Perikarderguss caused by inflammation of the pleura, which is adjacent to the pericardium, a pericardial effusion is often painless, but when it occurs in acute pericarditis, pain may be present. Significant amounts of pericardial fluid can be made to disappear, increase the range of cardiac silence and change the size and shape of the cardiac silhouette the heart sounds. A pericardial rub may be heard. In large pericardial effusions, the compression of the left lung, the breath sounds decrease (to hear near the left scapula) and crackling cause. The arterial pulse Jugularvenenpuls and blood pressure are normal until the intrapericardial pressure increases significantly, leading to tamponade. When Postmyokardinfarktsyndrom a pericardial effusion with fever, friction rub, pleurisy, pleural effusion and joint pain may occur. This syndrome is usually formed within ten days to two months after myocardial infarction. It is usually mild in intensity, but can also be pronounced. Sometimes it comes from one to ten days after myocardial infarction and more common in women to a Herzmuskelruptur that verursacht.Herzbeuteltamponade a haemopericardium and a tamponade Clinical findings are similar to those in cardiogenic shock: debased cardiac output, low systemic arterial blood pressure, tachycardia, and dyspnea. The neck veins are significantly dilated. A severe cardiac tamponade is almost always associated with a decrease in systolic blood pressure> 10 mmHg during inspiration (paradoxical pulse). In advanced cases, the pulse can disappear during inspiration (a paradoxical pulse may even in COPD, bronchial asthma, a pulmonary embolism, a right ventricular infarction and a nichtkardiogenem shock may occur). The heart sounds disappear, except for a small effusion. Chambered effusions and eccentric or localized hematoma can cause a localized tamponade, be in only selected ventricles compressed. In these cases, physical, hemodynamic and some echocardiographic signs fehlen.Konstriktive pericarditis can Fibrosis or calcification rarely causes symptoms, except when a constrictive pericarditis develops. The only early change may be an increased diastolic ventricular, atrial, pulmonary or systemic venous pressure. Symptoms and signs of peripheral venous congestion (eg., Peripheral edema, jugular veins congestion, hepatomegaly) may occur together with an early diastolic heart sound (pericardial knock), which is best heard during inspiration. This sound is caused by the sudden decrease in diastolic ventricular filling due to the stiff pericardium. The systolic left ventricular function (as measured by ejection fraction) is typically obtained. A sustained increase in pulmonary venous pressure leading to dyspnoea (v. A. At effort) and orthopnea. The fatigue can be pronounced. A widening of the neck veins by an increase in venous pressure during inspiration is present (Kussmaul-mark); This is absent in cardiac tamponade. A paradoxical pulse is rare and usually less pronounced than in tamponade. The lungs are not jammed, unless it develops a severe left ventricular constriction. Diagnostic ECG and chest X-ray echocardiography tests to identify the cause (z. B. aspiration of pericardial fluid, Perikardbiopsie) ECG and chest X-ray are performed. An echocardiography is performed to an effusion (particularly a chambered effusion with localized tamponade, which is not suspected because of their atypical manifestations and due to indirect evidence, such as chamber compression and characteristic respiratory variations obvious is), cardiac Füllanomalien and wall motion abnormalities which are characteristic for assistance from the myocardium to consider. Blood tests may reveal leukocytosis and a reduction acceleration, but these findings are nonspecific. Acute pericarditis The diagnosis is made due to the presence of the following clinical and ECG changes that are not always present in all cases. Characteristic chest pain Pericardial friction ECG abnormalities pericardial Serial ECGs may be necessary to detect the changes. The ECG in acute pericarditis may include changes in the ST and PR-segment and the T-waves, typically in most derivatives. (ECG changes in leads aVR generally take place in the opposite direction to the other derivatives) Unlike the myocardial infarction pericarditis does not cause any contralateral reductions of the ST segment (except in leads aVR and V1) and there is no pathological Q- Pink. ECG changes in pericarditis can occur in four stages, although not all levels are available in all cases. Stage I: ST-segments show upward concave elevation; The PR-segments are pressed (acute pericarditis: EKG stage 1) Step II: ST-segments go back to the base line; T waves flatten. Stage II: T-waves may be inverted T-wave inversion occurs on only after the ST segment has returned to normal, and is different from the appearance of acute ischemia or myocardial infarction in all leads. Stage IV: T-wave changes solve Echocardiography shows in acute pericarditis usually a pericardial effusion, which the diagnosis can be confirmed; contrast echocardiography often appears normal in patients with pure fibrinous acute pericarditis. Among the findings that indicate myocardial involvement, including local or diffuse left ventricular dysfunction. Acute pericarditis: EKG stage 1 ST-segments, with the exception of aVR and V1 show an upwardly curved survey. T waves are essential normal PR segments except aVR and V1. Since the pain of pericarditis can be very similar to that in acute myocardial infarction, or in pulmonary infarction, additional investigations (eg. As cardiac enzymes in the serum, CT of the lungs) may be necessary if the history and ECG findings of pericarditis are atypical , Troponin is often elevated in acute pericarditis due to epicardial inflammation, so it can not differentiate between pericarditis, acute myocardial infarction and pulmonary embolism. Very high Troponinlevel may indicate a myopericarditis. The CK level, which is less sensitive than the Troponinlevel is usually normal in acute pericarditis unless myocarditis present. The Postperikardiotomie- and Postmyokardinfarktsyndrome can be difficult to detect and have to be distinguished from a recent myocardial infarction, pulmonary embolism and in front of a peripheral infection after surgery. Pain, friction rub, and fever, up to several months to occur two weeks after surgery and quickly respond to the administration of aspirin, nonsteroidal anti-inflammatory drugs, colchicine or corticosteroids help in Diagnosestellung.Perikarderguss The suspected diagnosis is made in the presence of clinical findings , but is often discovered only after an vergößerten cardiac silhouette in the chest x-ray image. The ECG often finds a QRS voltage, sinus rhythm is maintained at about 90% of patients. For large chronic effusions, the ECG may demonstrate an electrical alternans (z. B. increased and the amplitude of the P, QRS or T-wave is lowered in alternating heartbeats). An electrical alternans is connected with changes in heart position (swinging heart). Echocardiography estimates the volume of pericardial fluid, identifies a cardiac tamponade, acute myocarditis and / or heart failure and can provide information about the cause of pericarditis. Patients with normal EKG, pericardial effusion small (<50 ml) and without any suspicious findings on the medical history and in the investigation can be observed in the serial examinations and with echocardiography. Other patients need to be studied further to the etiology to bestimmen.Konstriktive pericarditis The diagnosis may be due to clinical, ECG, the chest x-ray absorption and Doppler echocardiographic findings are made, but a cardiac catheterization and CT (or MRI) are usually required. Rarely is necessary to exclude a restrictive cardiomyopathy, a biopsy of the right ventricle. The ECG -Changes are nonspecific. The QRS amplitude is usually low. T-wave changes are usually nonspecific. Atrial fibrillation occurs in about one third of patients, atrial flutter is rare. A lateral chest x-ray image shows the pericardial calcifications often best, but these findings are nonspecific. Echocardiography is also non-specific. When the right and left Ventrikelfüllungsdrücke have increased about the same, the Doppler echocardiography helps to distinguish constrictive pericarditis from restrictive cardiomyopathy. During inhalation, the diastolic mitral flow velocity drops> 25% in constrictive pericarditis but <15% at the restrictive cardiomyopathy. In constrictive pericarditis, the inspiratory flow rate increases over the tricuspid valve more than normal, this is not the case with restrictive cardiomyopathy. The determination of tissue velocities at the mitral annulus can be helpful if excessively high left atrial pressures disappear the respiratory function of the transvalvular flow rates. Cardiac catheterization, right and left side, occurs when suggestive clinical and echocardiographic findings in a constrictive pericarditis. A cardiac catheterization helps the abnormal hemodynamics to confirm and quantify that defines the limited pericarditis: The mean pulmonary artery occlusion pressure (PCWP, pulmonary capillary wedge pressure), diastolic pulmonary artery, the right ventricular end-diastolic pressure and mean right atrial pressure are all approximately 10-30 mmHg. The pulmonary artery and right ventricular systolic pressure are increased normal or slightly so that the pulse amplitudes are small. In the atrial pressure curve of the x and y -Slope -Slope are typically highlighted. In the ventricular pressure curves diastolic waste the time of rapid ventricular filling occurs. During the high point of inspiration, right ventricular pressure rises when the left ventricular pressure is lowest (sometimes called a mirror image unconformity, which increased ventricular interdependence implies). Since the ventricular filling is limited, the Ventrikeldruckkurven show a sudden fall followed by a plateau (similar to a root character) in early diastole The measurement of these changes requires a simultaneous right and Linksherzherzkatheterisierung with separate signal transmitters. These hemodynamic changes almost always occur in a significant constrictive pericarditis, but may be masked during hypovolemia. Right ventricular systolic pressures> 50 mmHg often occur at a restrictive cardiomyopathy, but less common in constrictive pericarditis on a. If the PCWP corresponds to the mean right atrial pressure and a drop of the early diastolic Ventrikeldruckkurve occurs with large x and y -waves in the right atrial curve, each of the two diseases may be present. CT or MRI can detect a Perikardverdickung of> 5 mm. > 5 mm thickening, along with typical hemodynamic changes (evaluated by echocardiography and catheterization) can confirm the constrictive pericarditis. If no pericardial thickening or fluid is seen, the diagnosis of restrictive cardiomyopathy is favored, but this is not certain. A normal pericardial thickness does not exclude a constrictive pericarditis. A cardiac MRI, in particular the degree of gadolinium increase in the pericardium, may help to identify patients in which those temporary narrowing or dissolve wird.Herzbeuteltamponade A low voltage and electrical alternans on the ECG suggest a cardiac tamponade, but lacks these findings the sensitivity and specificity. When a tamponade is suspected, an echocardiogram is performed, unless that even a short delay is life-threatening. Then a pericardiocentesis is performed to diagnose and treat. In the echocardiography a breathing function of transvalvular and venous flow and the compression or collapse of the right ventricle in the presence of a pericardial effusion for this diagnosis speak. Tips and risks Significant cardiac tamponade is a clinical diagnosis, echocardiographic findings alone are not indicative of a Perikardpunktion. When a tamponade is suspected, a right heart (Swan-Ganz) can be performed. In pericardial tamponade: There is no early diastolic ventricular pressure drop in the recording. Diastolic pressures are elevated (about 10-30 mmHg) and the same in all chambers of the heart and the pulmonary artery. In the atrial pressure curve of xAbfall is preserved and the y -Slope lost. In contrast, exceeds heavy Stauungszuständen due to dilated cardiomyopathy the pulmonary artery occlusion pressure or LV end-usually the mean right atrial and right ventricular pressure by ? 4 mmHg.Diagnostik the causes After pericarditis is diagnosed, studies to determine the etiology and impact are performed on cardiac function. In a young, previously healthy adults who presents with a viral infection and acute pericarditis, an extensive investigation is usually unnecessary. The differentiation of viral from idiopathic pericarditis is difficult, expensive and usually of little practical significance. A biopsy of pericardial tissue and aspiration of the pericardial fluid may be necessary in other cases to establish the diagnosis. Acid-resistant patches and pericardial fluid cultures are essential if TB is considered possible (TB-pericarditis can be aggressive and rapidly deteriorate at a corticosteroid treatment). The samples are tested for the presence of malignant cells. A complete drainage of a newly identified pericardial effusion is usually unnecessary for diagnosis. A persistent (usually> 3 months) or progressive effusion also requires pericardiocentesis if the etiology is unclear. The choice between a Nadelperikardpunktion and a surgical drainage depends on the institutional, medical experience, the etiology of the effusion, the need for diagnostic tissue samples and the prognosis of the patient. A Nadelperikardpunktion is often best if the etiology is known and the presence of tamponade is considered. A surgical drain is best if the presence of tamponade is safe, but the etiology unclear. The laboratory tests of pericardial fluid, which go beyond the culture and cytology, are usually non-specific. but a specific diagnosis is sometimes possible when newer visual, cytological and immunological analysis of the liquid to be carried out, which was won by a perikardioskopisch guided biopsy. A cardiac catheterization may be useful to examine the pericarditis and identify the cause of the decreased heart function. CT or MRI can help detect metastases, although an echocardiogram is often sufficient. Other studies include blood counts, acute phase proteins, routine examination of clinical chemistry, cultures, autoimmune tests and, when indicated, testing for HIV infection, histoplasmosis complement fixation (in endemic areas), and antibody tests for coxsackievirus, influenza virus, echovirus and streptococci. Studies on anti-DNA and anti-RNA antibodies can be helpful. A PPD skin test is performed, but it may provide a false negative result. A TB pericarditis can be ruled only by cultures of the pericardial fluid for acid-fast bacilli. Treatment varies depending on the cause NSAIDs, colchicine and sometimes corticosteroids for pain and inflammation

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