pericarditis

Introduction

Introduction to pericarditis There are two layers of pericardium in the visceral and parietal layers outside the heart. If they have inflammatory changes, they are pericarditis, which can limit the pressure and relaxation of the heart. Pericarditis can be divided into acute and chronic, and the most serious type of chronic pericarditis is constrictive pericarditis. Classification of pericarditis acute pericarditis: symptoms can be caused by primary diseases, such as tuberculosis can have hot flashes in the afternoon, night sweats. Suppurative pericarditis can have chills, high fever, and sweat. Inflammation of the pericardium itself can show pain in the back of the chest, difficulty breathing, coughing, hoarseness, difficulty swallowing, etc. In the early stage of acute pericarditis and in the late stage of pericardial effusion absorption, pericardial friction sounds can be heard in the anterior region of the heart, which can last from several hours to several days. When the amount of pericardial effusion exceeds 300 ml, the apical beat can disappear. A significant reduction in cardiac output can cause shock. Diastolic relaxation is limited, so that increased venous pressure can produce jugular vein engorgement, hepatomegaly, ascites, lower extremity edema, and odd veins. Constrictive pericarditis: The cause of this disease is mostly tuberculosis, followed by purulent. After acute pericarditis, it usually takes 2-8 months to have obvious signs of pericardial constriction. Acute narrowing occurs within one year after acute pericarditis, and is chronically narrowed in one year. Mainly manifested as dyspnea, apical beat weakened or disappeared, jugular vein engorgement, hepatomegaly, massive ascites and lower extremity edema, odd pulse. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: myocardial infarction

Cause

Cause of pericarditis

Pericarditis etiology

Autoimmune (20%):

Rheumatic fever and other collagen tissue diseases, such as systemic lupus erythematosus, nodular polyarteritis, rheumatoid arthritis; after heart injury, such as pericardial incision syndrome.

Infection (35%):

Acute pericarditis is often a manifestation or complication of other diseases. Mostly caused by infection, tuberculous, suppurative (cocci, pneumococcal) and viral.

Acute pericarditis

Acute pericarditis can be caused by infection, connective tissue abnormalities, metabolic abnormalities, injuries, myocardial infarction or certain drugs, or can be non-specific.

In acute pericarditis, the infection can be caused by bacteria, parasites, protozoa, viruses or fungi. Bacterial infections are more common in streptococcus, staphylococcus and gram-negative bacilli, and common causes of Haemophilus influenzae in children are suppurative pericarditis. Rarely, can occur in infective endocarditis, pneumonia, sepsis and penetrating injury; after cardiac surgery and patients with impaired immune function, viral infection is common with Echo, Influenza and Coxsackie B viruses In some cities, AIDS is the most common cause of pericardial effusion by echocardiography. AIDS can be caused by avian Mycobacterium tuberculosis actinomycetes, fungal or viral infections, lymphoma or Kaposi's sarcoma. Inflammation, but pericardial effusion often has no obvious cause. Tuberculous pericarditis is insidious and can be present without significant lung involvement. Tuberculous pericarditis accounts for only 5% of acute and subacute pericarditis in the United States, but is predominant in some parts of India and Africa.

Acute or chronic pericarditis can also be caused by connective tissue (autoimmune) abnormalities such as rheumatoid, systemic lupus erythematosus, scleroderma and metabolic abnormalities such as uremia, which can also occur due to injury; Pericardial incision syndrome, accounting for 5% to 30% of cardiac surgery, chest penetration or non-penetrating injury can cause pericardial hemorrhage leading to pericarditis (sometimes leading to pericardial tamponade, cardiac catheter can penetrate the myocardium Pericardial cavity, saccular aortic aneurysm or dissecting aortic aneurysm can rupture into the pericardium.

Acute myocardial infarction 10%~15% may have acute pericarditis in the early stage, and late post-infarction syndrome (Dressler syndrome) usually occurs in 10 days to 2 months after infarction, and the incidence rate is 1% to 3%. Fever, pericarditis with pericardial friction, pericardial exudation, pleurisy, pleural effusion and joint pain, occasional heart rupture after myocardial infarction, causing pericardial hemorrhage, which usually occurs 1 to 10 days after infarction, more women than men,

Acute pericarditis can be complicated by certain drug treatments such as procainamide, hydralazine, isoniazid, methimylgye, phenytoin or anticoagulant, sometimes the cause of acute pericarditis cannot Certainly, it is called non-specific pericarditis, but some cases are confirmed to be caused by viruses in the future.

Chronic pericarditis

The main subtypes are chronic constrictive pericarditis and chronic exudative pericarditis.

Chronic constrictive pericarditis is usually non-specific, but almost any acute pericarditis can be the cause, common causes are tuberculosis or other infections, new organisms, sunlight or sound radiation, rheumatoid arthritis, trauma and heart Surgery, there is very little constrictive pericarditis after rheumatic fever,

Chronic exudative pericarditis is usually non-specific, but can be caused by Mycobacterium tuberculosis, fungi or new organisms. The most common cause of massive pericardial exudation in hospitalized patients is metastatic tumors such as cancer (especially lung cancer or breast cancer). ), sarcoma (especially melanoma), leukemia, lymphoma, direct spread of thoracic tumors can also occur; pericardial primary mesothelioma is rare, tumor may invade the pericardium may have serous or bloody exudation, can be Limitations or extensiveness; if extensive cerebral tamponade can occur, obstructing cardiac function,

Fibrinous pericarditis

Fibrinous pericarditis: acute fibrin exudation, with inflammatory cells and a small amount of endothelial cells exudation, no obvious fluid exudation, commonly known as "dry pericarditis."

The performance of fibrinous pericarditis: 1 chest pain, sharp pain, also pressure-like, located in the anterior region, related to breathing, body position; 2 fever; 3 typical signs: pericardial friction sound.

In the past, common diseases were due to rheumatic fever, tuberculosis and bacterial infections. In recent years, the incidence of viral infections, tumors, and myocardial infarctitis has increased significantly.

(A) symptoms of precordial pain in the main area, such as acute non-specific new pericarditis and infectious pericarditis; slow development of tuberculous or neoplastic pericarditis pain symptoms may not be obvious. The nature of the pain can be sharp, related to respiratory movements, often aggravated by coughing, deep breathing or changing position; in the anterior region, it can be radiated to the neck, left shoulder, left arm and left shoulder tibia, but also to the upper abdomen; pain can also be Pressed, located behind the sternum. The precordial pain caused by this disease may be similar to the pain of myocardial infarction, and attention should be paid to the identification.

(B) physical signs pericardial friction sound is a typical sign of fibrinous heart disease, the wall layer and the visceral layer which become rough due to inflammation occur when the heart is moving together, and it is scratched and rough, which is not related to the occurrence of heart sound. Sexuality, often over the heart sound and closer to the ear than the heart sound, the typical friction sound can hear the three components of atrial contraction, ventricular contraction and ventricular relaxation, but most of them are only biphasic that is roughly consistent with atrial contraction and relaxation. Friction sound; mostly located in the anterior region, the most obvious between the 3rd and 4th ribs on the left sternal border. When sitting, the body leans forward, deep inhales or presses the chest to make it easier to hear. The pericardial friction sound can last for several hours or last for several days or weeks; when the effusion increases and the second layer of pericardium is separated, the rubbing sound disappears, but if some of the pericardial adhesions are still audible. The heart area can be diagnosed by hearing the pericardial friction sound.

Pathophysiology

Acute pericardium: acute pericarditis can be serous, fibrinous, hemorrhagic or suppurative. The surface layer of the subepicardial myocardium may be involved, and the amount and nature of the cellular response depends on the cause.

Chronic pericardium: Chronic pericarditis can be serous, chylorrhotic or bloody (exudative), or fibrous, adhesion or calcification. It can be constricted or does not produce clinical symptoms, pericardial fibrosis can be infected, damaged or pericardial Produced by blood, or with connective tissue diseases, including rheumatic fever, but sometimes the cause is unknown. Fibrosis may be spotted or extensive, with calcareous deposition, pericardial fibrosis may have no hemodynamic effect, and may gradually produce chronic Constrictive pericarditis causes chronic increase in systemic venous pressure and hepatic venous pressure, leading to cardiogenic cirrhosis.

In chronic exudative pericarditis, pericardial exudate is about 50ml~1L (normal <25ml). Pericardial exudate is small, but it produces fast, or produces slow and large amount, or due to fibrosis, calcification or new organisms make pericardium Reduced compliance can limit the filling of the ventricle during the expansion phase. In this case, the left ventricular end-diastolic pressure is determined by the amount of pericardial exudation and the degree of pericardial thickening. The diastolic blood pressure values of the ventricle, atrium and venous bed are close, usually 13~32mmHg, systemic venous stagnation occurs, excessive body fluid leaks from the capillaries, postural edema, ascites in the later stage, and signs of stagnation in the surrounding tissue are more severe than lung stagnation The blood is obvious, and the pulmonary edema with obvious symptoms is not common, but the pericardial effusion gradually develops, even if >1L can not produce tamponade symptoms, because the pericardium can be stretched to adapt.

Prevention

Pericarditis prevention

Pericarditis prognosis

Rheumatic and non-specific pericarditis rarely cause pericardial tamponade and constrictive pericarditis, tuberculous, suppurative and radiation-induced pericarditis are more likely to develop into constrictive pericarditis, so early diagnosis and timely treatment should be prevented to prevent development.

Complication

Pericarditis complications Complications, myocardial infarction

The following complications can occur:

Pericarditis after acute myocardial infarction is divided into early types of pericarditis, Dressler syndrome and rupture of ventricular free wall:

1. A subgroup analysis of early-stage pericarditis GISSI studies showed that thrombolytic therapy reduced the incidence of pericarditis from 12% to 6.7%. The earlier the treatment started, the lower the incidence of pericarditis. There was no significant difference in the incidence of dry pericarditis in different parts of the myocardial infarction. Pericardial effusion occurred mostly in the anterior wall myocardial infarction. The presence of pericardial effusion also indicated that the infarct size was larger. Several clinical studies have shown that myocardial infarction complicated with pericardial effusion is self-limiting and does not develop into tamponade, but Figueras reported that 92 of the 473 patients with myocardial infarction had moderate pericardial effusion (>10 mm), of which 60 Pericardial tamponade occurred, and 38 patients died of ruptured ventricular free wall. Multivariate analysis showed that early small amounts of pericardial effusion and age greater than 60 years were independent predictors of advanced moderate effusion and pericardial tamponade. According to reports, pericarditis after myocardial infarction in individual cases can develop into pericardial constriction. The hospital mortality rate of patients with myocardial infarction complicated with pericarditis is not higher than that without this complication, but the long-term prognosis may be poor. Widimsky reported a group of 3 years of follow-up data. Heart failure and mortality were 49% in patients with pericarditis, 16% in patients without pericarditis (P 0.01), and high in the former (15%: 8%). ), but no significant difference.

2. Dressler syndrome usually occurs 1 week to half a month after myocardial infarction, the incidence rate is 1% to 3%. Its pathogenesis is related to autoimmune and viral infections, and early pericarditis is more likely to occur after myocardial infarction. Dressler syndrome rarely occurs in a large number of pericardial effusions, cardiac tamponade and constrictive pericarditis, and individual patients can have repeated episodes several times.

3. Pericarditis caused by rupture of ventricular free wall caused by rupture of ventricular free wall is the most serious complication of myocardial infarction, and 50% often causes acute cardiac tamponade. Patients can suddenly coma, convulsions, heartbeat and respiratory arrest, the vast majority of rescue is difficult to succeed, the prognosis is very poor, accounting for 5% to 10% of patients with myocardial infarction, most of the patients are elderly, with a history of long-term hypertension, myocardial infarction Transmural, lack of collateral circulation. The use of steroids, inappropriate use of positive inotropic drugs, uncontrolled high blood pressure, premature physical labor and the use of anticoagulants are all possible causes. A small number of patients have small ruptures and form pseudo-ventricular aneurysm. In such patients, the survival rate can reach 48.5%. If the operation is delayed, the pseudo-ventricular aneurysm can be further expanded and ruptured, and blood enters the pericardial cavity, causing cardiac tamponade. And death.

Symptom

Pericarditis symptoms Common symptoms Fever with cough, slightly... Hepatomegaly Ascites pale pale night sweats diarrhea, breathing difficulties, cardiovascular and cerebrovascular accidents

Patients may have fever, night sweats, cough, sore throat, or vomiting or diarrhea. Acute heart tamponade can occur when the pericardium quickly exudes a large amount of fluid. The patient has chest pain, difficulty breathing, cyanosis, pale complexion, and even shock. There may also be ascites, hepatomegaly and other symptoms.

Examine

Pericarditis check

Pericardial physicochemical examination

X-ray examination: When the amount of fluid exceeds 300 ml, the heart shadow increases to both sides, and the angle of the heart becomes an acute angle. At more than 1000 ml, the heart shadow is in the form of a flask and varies with body position. The heart beats weakened or disappeared.

Electrocardiogram: In the case of dry pericarditis, each lead (except avR), the ST segment is raised, and returns to the equipotential line after a few days, and the T wave is flat or inverted. When the pericardium has exudate, the QRS complex is low voltage.

Echocardiography: It shows an illuminating dark area in the pericardial cavity, which is an accurate, safe and simple diagnostic method.

At present, the treatment of this disease is still based on the treatment of primary disease. If necessary, symptomatic treatment measures can be taken. For example, chest pain can be given painkillers. If the amount of pericardial effusion is large, it can be used for pericardial puncture.

Chinese medicine believes that this disease is mostly caused by "heartache", "chest", "sipping", "edema" and other diseases. The incidence, especially the pericardial effusion and the spleen and stomach damage, water wet stop, block in the heart envelope. The water drink is stopped in the pericardium, but it can be forced into the heart and forced to the lungs, causing asthma and discomfort. Therefore, when treating, it is necessary to go to the water to drink the evil, and the water goes to its breath and self-leveling.

The inflammation of the pericardium can be acute or chronic and can lead to exudation of the pericardium.

Diagnosis

Diagnosis and diagnosis of pericarditis

Clinical manifestation

Acute pericarditis is divided into fibrin and exudative.

Fibrinous pericarditis: Pain in the precordial area is the main symptom of pain. The nature of the pain can be sharp and related to respiratory movement. It is often aggravated by coughing and deep breathing to change position or swallowing. It can be radiated to the left anterior and left scapula of the neck. Upper abdomen; pain can also be squeezed. The precordial pain caused by this disease after the sternum may be similar to the pain of myocardial infarction.

Exudative pericarditis: clinical manifestations depending on the degree of tamponade of the effusion to the heart can still maintain normal hemodynamics, circulatory disorder or failure dyspnea is the most prominent symptom of pericardial effusion may be Bronchopulmonary compression and pulmonary congestion related to severe dyspnea, the patient is sitting and breathing, leaning forward, breathing shallow, pale, pale, may have blemishes, may also cause dry cough due to compression of the tracheal esophagus, hoarseness and difficulty in swallowing, and may have chills and fever The front area or upper abdomen is swelled and fatigued.

Cardiac tamponade: rapid pericardial effusion can cause acute cardiac tamponade, obvious tachycardia, decreased blood pressure, decreased pulse pressure, and a significant increase in venous pressure. If the cardiac output is significantly decreased, acute circulatory failure can occur.

diagnosis

According to the clinical manifestations of X-ray electrocardiogram and echocardiography, the diagnosis of pericarditis can be made and then the etiology of different etidal pericarditis and pericardial biopsy should be combined to diagnose the etiology.

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