Diagnosis of pericarditis
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
A presumptive diagnosis of pericarditis can be made on the basis of ECG data, chest X-ray and Doppler echocardiography, but to clarify it, heart and CT (or MRI) are probed. Because ventricular filling is limited, the ventricular pressure curves show a sudden drop, accompanied by a plateau (resemble a square root) in early diastole. Sometimes there is a need for a right ventricular biopsy to exclude restrictive cardiomyopathy.
Changes in the cardiogram are nonspecific. The voltage of the QRS complex is usually low. Teeth T is usually nonspecifically altered. Atrial fibrillation develops in about a third of patients. Atrial flutter is less common.
X-ray images in the lateral projections often show calcification, but the findings are not specific.
Changes on the echocardiogram are also nonspecific. When the filling pressure of the right and left ventricles are equally elevated, Doppler echocardiography helps distinguish constrictive pericarditis from restrictive cardiomyopathy. During inspiration, the rate of mitral diastolic flow falls by more than 25% with constrictive pericarditis, but less than 15% with restrictive cardiomyopathy. With constrictive pericarditis, the speed of the tricuspidal flow on inspiration increases more than usual, but this does not occur with restrictive cardiomyopathy. The determination of the speeds of movement of the tissues of the vital ring can help when excessively high pressure in the left atrium levels out the respiratory changes in the transflected velocities.
If clinical and echocardiographic data are indicative of constrictive pericarditis, heart probing is performed. It helps to confirm and determine the quantitatively altered hemodynamics, which is characteristic of constrictive pericarditis: the value of pulmonary wedge pressure (pulmonary capillary jam pressure), diastolic pressure in the pulmonary artery, right ventricular pressure at the end of the diastole, right atrial pressure (all within 10-30 mmHg.). Systolic pressure in the pulmonary artery and right ventricle is normal or slightly elevated, so the pulse pressure is low. In the pressure curve in the atria, waves x and y are typically amplified; in the ventricular pressure curve, a diastolic decrease occurs during the phase of rapid ventricular filling of the ventricles. These changes are almost always detected with severe constrictive pericarditis.
Systolic pressure in the right ventricle> 50 mm Hg. Art. Often recorded with restrictive cardiomyopathy, but less often with constrictive pericarditis. When the pulmonary artery wedge pressure equals the mean right atrial pressure and the early diastolic pressure decrease in the intraventricular pressure curve leads to the formation of large waves x and y on the right atrial pressure curve, any of the above diseases can be present.
CT or MRI helps to identify the thickening of the pericardium more than 5 mm. Such data with typical changes in hemodynamics can confirm the diagnosis of constrictive pericarditis. When pericardial thickening or effusion is not detected, restrictive cardiomyopathy is diagnosed, but this is not proven.
Etiological diagnosis. After the diagnosis of pericarditis, studies are conducted to identify the etiology and influence on cardiac function. In young, previously healthy people who underwent a viral infection and subsequently pericarditis, volumetric diagnostic search is usually not advisable. Differential diagnosis of viral and idiopathic pericarditis is difficult, expensive and does not have much practical significance.
A pericardial biopsy or aspiration of pericardial effusion may be necessary to establish a diagnosis. Staining with acid dyes and microbiological examination of the pericardial fluid help in identifying the causative agent of the infection. In addition, the samples are examined for the presence of atypical cells.
However, the complete removal of newly identified pericardial effusion is usually not required for diagnosis. Persistent (present for more than 3 months) or progressive effusion, especially when etiology is not established, is an indication for pericardiocentesis.
The choice between puncture pericardiocentesis and surgical drainage depends on the physician's capabilities and experience, the etiology, the need for diagnostic tissue samples and the prognosis. Puncture pericardiocentesis is considered preferable when etiology is known or the possibility of cardiac tamponade is not ruled out. Surgical drainage becomes the method of choice if the presence of tamponade is proven, but the etiology is unclear.
The data of laboratory studies of pericardial fluid, except for culture and cytology, are usually nonspecific. But in certain cases it is sometimes possible to use new visualizing, cytological and immunological methods of fluid obtained during biopsy under the control of pericardioscopy.
Cardiac catheterization is used to assess the severity of pericarditis and to establish the cause of a decline in heart function.
CT and MRI can help in detecting metastases, although usually echocardiography is usually sufficient.
Other studies include a general blood test, determination of acute inflammatory phase markers, a biochemical blood test, culture testing, autoimmune tests. If necessary, an HIV test, complement fixation reaction for histoplasmosis (in endemic areas), streptolysin analysis and antibodies to Coxsackie, influenza and ECHO viruses are performed. In some cases, anti-DNA, anti-RNA antibodies are determined and skin test for sarcoidosis is performed.
[