Acute pericarditis

Introduction to acute pericarditis Acute pericarditis (acutepericarditis) is a syndrome caused by acute inflammation of the visceral and parietal layers of the pericardium. Clinical features include chest pain, pericardial friction and a series of abnormal electrocardiogram changes. The clinical manifestations of acute pericarditis are insidious and easily missed. Acute pericarditis has many causes, which can be from the pericardium itself, or it can be part of systemic diseases. It is clinically tuberculous, non-specific, and neoplastic. Systemic diseases such as systemic lupus erythematosus and uremia Such lesions are easy to get involved in the pericardium caused by pericarditis. basic knowledge The proportion of illness: 0.0002% Susceptible people: no specific population Mode of infection: non-infectious Complications: arrhythmia myocardial ischemia chronic constrictive pericarditis

Cause of acute pericarditis

Infection factor (30%):

Bacterial: (1) suppurative pericarditis; (2) tuberculous pericarditis.

Viral: Pericarditis caused by Coxsackie, Echo, Influenza, and Cytomegalovirus.

Fungal: such as histoplasma, actinomycetes, nocardia, auricularia, mycobacteria, and the like.

Others: such as rickettsia, spirochete, mycoplasma, paragonimiasis, amoeba and cysticercosis.

Disease factors (20%):

Autoimmune diseases: such as rheumatic fever, rheumatoid arthritis, systemic lupus erythematosus, dermatomyositis, scleroderma, polyarthritis, post-cardiac incision syndrome, post-myocardial infarction syndrome, dialysis treatment, kidney Transplantation and AIDS.

Allergic diseases: such as serum diseases, allergic granuloma and allergic pneumonia.

Diseases in adjacent organs: such as myocardial infarction, dissecting aneurysms, pulmonary embolism, pleura, lung and esophageal diseases.

Endocrine and metabolic diseases: such as uremia, mucinous edema, diabetes, gout, Axon disease, cholesterol pericarditis, etc.

Others: such as pancreatitis, thalassemia, intestinal fat metabolism disorders, non-gonococcal arthritis, conjunctiva, urethritis syndrome, etc.

Physical factors (5%):

Trauma such as penetrating wounds, foreign bodies, cardiac catheters, artificial pacemakers, and heart massage.

Drug factor (5%):

Such as hydralazine, procainamide, phenytoin, penicillin, isoniazid, phenylbutazone and methylthiouracil.

Other factors (20%):

Acute non-specific pericarditis is a serous fibrinous pericarditis. The cause is unknown. It may be related to viral infection or allergies and autoimmune reactions. It is more common in men and young adults. Primary mesothelioma, sarcoma, etc. Metastasis of secondary lung or breast cancer, multiple myeloma, leukemia and lymphoma can lead to acute pericarditis.

Pathogenesis

1. Pathological anatomy: pathological changes of acute pericarditis. The early manifestations are the inflammatory reaction of the visceral and parietal layers of the pericardium. A viscous liquid containing fibrin deposition and polynuclear leukocyte aggregation is called fibrinous or dry pericarditis. Due to the different causes or progress of the disease, the fluid in the exudate increases, the amount of fluid can be as much as 2 ~ 3L, called exudative or wet pericarditis, the exudate of pericarditis can be fibrin, serous blood or Suppurative and so on.

The inflammatory reaction often involves the myocardium in the lower part of the pericardium. A few severe cases may involve the deep myocardium, which is called myocardial pericarditis. After the pericarditis is healed, small plaques may remain or different degrees of adhesion may remain. If the inflammation involves the outer surface of the pericardial wall layer, Produces adhesion between the heart and adjacent tissue pleura, mediastinum and diaphragm, exudate of acute fibrinous pericarditis, often completely dissolved and absorbed, or longer-term existence; can also be mechanized, replace scars for connective tissue, and even cause pericardium Calcification eventually develops into a constrictive pericarditis.

2, pathophysiology: acute fibrinous pericarditis does not affect hemodynamics, and pericardial effusion is the main cause of a series of pathophysiological changes caused by acute pericarditis, if the exudate progresses slowly, due to excessive pericardial extension, pericardial cavity Although it can accommodate 1~2L of liquid without increasing the pressure inside the pericardium, this kind of pericardial effusion without cardiac tamponade or pericardial tamponade can have no clinical symptoms. If the exudate is rapidly or massively accumulated, the pressure in the pericardial cavity will rise. When a certain degree is reached, the heart is dilated, the ventricular diastolic filling is reduced, and the stroke volume is reduced. At this time, the body's compensatory mechanism increases the ventricular filling by increasing the venous pressure, increasing the myocardial contractility to increase the ejection fraction, and accelerating the heart rate. Increase cardiac output; increase peripheral arteriolar resistance to maintain blood pressure, such as pericardial effusion continues to increase, pericardial pressure further increased to right atrial right ventricular diastolic blood pressure level, when the pressure difference is equal to zero, cardiac tamponade or pericardial tamponade It can happen that once the pericardial pressure and right ventricular pressure rise to the left ventricular diastolic pressure level, the above compensatory mechanism is exhausted and a distinct heart appears. The performance of the tamponade, that is, the elevated venous pressure can not increase the filling of the ventricle, and the ejection fraction is thus reduced; the heart rate of the overspeed shortens the ventricular diastolic phase and reduces the filling, and the cardiac output decreases; the arteriolar contraction reaches the limit, the artery The pressure drops to circulatory failure, which produces cardiogenic shock.

Acute pericarditis prevention

Active control of tuberculosis and HIV epidemics can significantly reduce the incidence of tuberculosis and HIV-associated pericarditis. Early coronary reperfusion therapy in patients with acute myocardial infarction can reduce the incidence of infarct size and pericarditis, actively treat various kidney diseases and prevent development. End-stage renal disease is the most cost-effective measure to reduce uremic pericarditis. Once acute pericarditis occurs in various diseases, there is no effective measure to prevent it from developing into pericardial effusion or pericardial tamponade.

Acute pericarditis complications Complications arrhythmia myocardial ischemia chronic constrictive pericarditis

1, cardiac tamponade: is a critical complication of pericardial disease. Acute pericarditis about 15% can occur cardiac tamponade.

2, cardiogenic cirrhosis: refers to the liver due to long-term congestion, hypoxia, liver cell atrophy, disappearance, cirrhosis caused by connective tissue hyperplasia, more common chronic constrictive pericarditis, accounting for cardiac origin 16.6% of cirrhosis.

3, arrhythmia: arrhythmia is one of the common complications of pericardial disease, its production and sympathetic excitation, atrial enlargement, epicardial inflammation, myocardial ischemia and mechanical compression.

4. Myocardial ischemia: There are occasional reports of myocardial ischemia in pericarditis, which may be related to coronary artery spasm, thickening of calcified pericardium, compression of coronary artery and reduction of coronary blood flow during cardiac tamponade.

Acute pericarditis symptoms Common symptoms Pericardial inflamed pericardial fibers thickened chest pain with dyspnea shoulders involved pain chest pain systolic and diastolic murmur chest tightness pale chest tightness hernia chest pain with chest tightness, heart palpitations

1, symptoms

(1) Chest pain: It is the main complaint of acute pericarditis. It is more common in the fibrin exudation stage of acute non-specific pericarditis and inflammatory changes of infectious pericarditis. The nature and location of the pain are variable, often located behind the sternum or The precordial area can be radiated to the neck and back, with sharp pain, even in the upper abdomen, similar to "acute abdomen", or similar to myocardial infarction ischemic pain, dull or crushing pain and radiated to the left Upper limbs, or tingling with each heartbeat, pain can be caused by two factors including pericardial and pleural inflammation, or may be related to pericardial distraction factors in pericardial effusion, pain in supine position, cough, deep suction When the gas is aggravated, it is relieved when leaning forward.

(2) Difficulty breathing: Dyspnea is the most prominent symptom of pericardial pericardial exudate. It is mainly to avoid the pericardial and pleural pain and produce a shallow breathing shift. Difficulty in breathing can also be caused by fever. A large amount of pericardial effusion leads to cardiac pressure. Plug, adjacent to the bronchi, lung tissue is stressed and aggravated, showing pale, irritability, chest tightness, sweating, etc., patients often take a seat, the body leans forward, so that the pericardial effusion down, forward shift To relieve the pressure on the heart and adjacent organs, thereby alleviating the symptoms.

(3) systemic symptoms: may be associated with potential systemic diseases such as tuberculosis, cancer, cough caused by uremia, cough, anemia, weight loss and other symptoms.

2, signs

(1) Pericardial friction sound: a specific sign of acute fibrinous pericarditis, which is caused by the friction between the wall layer and the visceral pericardium which are caused by the friction between the heart and the heart during the activity of the heart. The high-frequency sounds often overwhelm the heart sounds and have a heart-like sound that is closer to the ear. The traditional description of pericardial friction sounds is composed of three components, atrial pericardial contraction, ventricular contraction, and early ventricular diastolic blood filling. Most common, accounting for more than half, the round-trip two-phase friction sound associated with ventricular contraction and relaxation, and the single-phase systolic pericardial friction sound is more easily heard during or after the pericarditis.

The pericardial friction sound is characterized by a transient change. Usually, a diaphragm-shaped chest piece is used between the 3 to 4 intercostals of the left sternal border, the lower sternum and the vicinity of the xiphoid. The intensity is affected by the breathing and posture, and deep inhalation or forward tilting. The frictional tone of the sitting position is enhanced and can last for several hours, several days, several weeks. When there is exudation in the heart bag, when the two layers of pericardium are completely separated, the pericardial friction sound disappears; if the two layers of pericardium have partial adhesion, although there is pericardial effusion, Sometimes it is still audible and the rubbing sound is easy to be confused with the pleural friction sound or the squeaky sound produced by the unstressed skin during the use of the stethoscope; the single-phase pericardial friction sound needs to be reversed with the tricuspid or mitral regurgitation Noise identification.

(2) pericardial effusion: the appearance of symptoms is related to the amount and speed of effusion, but has nothing to do with the nature of the effusion. When the pericardial effusion reaches 200-300ml or more or the effusion accumulates rapidly, the following signs appear:

1 cardiac signs: heart beats weakened or disappeared, the heart sounds the sound boundary to the sides, the relative voiced sounds disappeared, the heart sounds light and far, the heart rate is fast, a few people can hear the early diastolic extra tone between the 3 ~ 4 intercostals of the left sternal border ( Pericardial slamming sound), this sound is 0.1 to 0.13 s after the second heart sound, high-profile slap shot, is due to the limitation of pericardial effusion during ventricular relaxation, the sudden termination of blood to form a vortex and impact on the ventricular wall to produce vibration.

2 left lung compression signs: a large number of pericardial effusion, the heart shifts to the left, oppressing the left lung, causing left lower lobe atelectasis, lung consolidation in the left scapular region, called Ewart sign.

3 cardiac tamponade signs: a large number of pericardial effusion or effusion accumulate quickly, even if the effusion only 150 ~ 200ml, causing the pericardial pressure more than 20 ~ 30mmHg can produce acute pericardial tamponade, manifested as tachycardia, cardiac palpitations Decreased amount, cyanosis, difficulty in breathing, decreased systolic blood pressure or even shock. If the effusion is a slow accumulation process, it can also produce chronic cardiac tamponade, which is marked by a significant increase in venous pressure, jugular vein engorgement and jugular vein dilation during inhalation. It is called Kussmaul sign, often accompanied by hepatomegaly, ascites and lower extremity edema. As the arterial systolic pressure decreases, the diastolic blood pressure changes little, the pulse is weak, the pulse pressure is reduced, and the odd pulse appears. The latter is mainly caused by the thoracic cavity. The blood flow is obviously changed with the breathing movement. The normal person produces negative pressure in the chest cavity during inhalation, the body venous return increases, the vascular volume in the thoracic cavity increases, the right heart discharge increases, the pulmonary venous blood flow and the left ventricular filling Decreased, causing arterial blood pressure to drop, but the extent of <10mmHg, no significant effect on peripheral arterial pulsation, and when a large number of pericardial effusion or cardiac tamponade, the negative pressure of the chest during inhalation Pulmonary vascular volume increased significantly, and the heart was limited by the effusion, the right ventricular filling and cardiac output could not be significantly increased, pulmonary venous return and left ventricular filling were significantly reduced, resulting in a significant drop in arterial pressure >10 mmHg.

Acute pericarditis

Acute pericarditis is often accompanied by non-specific inflammatory manifestations, including leukocytosis and increased erythrocyte sedimentation rate. Although myocardial enzymology is usually normal, elevated CK-MB can also occur in patients with acute pericarditis, ie it cannot be identified by CK-MB. Pericarditis and myocardial infarction, especially non-Q-wave myocardial infarction.

1. Electrocardiogram (ECG) examination

(1) In acute pericarditis, subendocardial myocardial involvement is the anatomical basis of ECG changes. The series of ECG examinations are important for the diagnosis of acute pericarditis. About 90% of patients with acute pericarditis have abnormal ECG changes. However, the typical series of ECG changes are only found in 50% of patients, which can be several hours to several days after the onset of chest pain. The typical evolution can be divided into four phases:

1 In addition to aVR and V1, all the ST segments of the lead are raised downwards, and the T wave is erect, usually lasting for several days, and disappears rapidly after less than 2 weeks.

2 After a few days of onset, the ST segment returns to the equipotential line and the T wave begins to flatten.

3 Except for the aVR and Vl leads, all lead T waves are symmetrically inverted and reach the maximum depth, but without the R wave voltage drop and pathological Q wave, which can last for several weeks, several months or longer.

4T waves are restored to erect, usually occurring within weeks or months, and certain tuberculous, uremic and neoplastic chronic pericarditis T wave inversions can be sustained.

(2) Other non-specific ECG changes in acute pericarditis include:

1PR segment shift: In addition to the aVR and V1 leads, the PR segment is depressed, suggesting that the subendocardial atrial muscle is damaged, which can be seen in about 80% of patients.

2QRS wave low voltage: It is caused by a large amount of pericardial effusion causing the influence of the current generated by the myocardium on the surface potential. The voltage can be recovered after the absorption of the exudate. If there is still a low voltage after the effusion, it should be considered with pericardial cellulose. The insulation is related to the surrounding tissue edema.

3 electric alternation: generally only see QRS wave group electric alternation, the whole P-QRS-T electric alternating change is a characteristic ECG performance of a large number of pericardial effusion; when a large number of pericardial effusion, the heart seems to be suspended in the liquid, so that normal rhythm activity The amplitude of myocardial oscillation is obviously increased, causing the alternating electrical axis of the heart to alternate with ECG. When the effusion is absorbed, the alternating phenomenon of electricity will disappear.

4 arrhythmia: sinus tachycardia is the most common, some may have atrial tachycardia, atrial flutter or atrial fibrillation, a small number of extensive myocardial inflammation or fibrosis may have atrioventricular block.

2, echocardiography

This is a simple, safe, sensitive and reliable non-invasive method for diagnosing pericardial effusion. It has been widely used in clinical practice. When M-mode echocardiography is performed, an anechoic zone (liquid dark area) can be seen to separate the myocardial echo from the pericardial echo. Open, this area is pericardial effusion, two-dimensional echocardiography to take the left heart long axis view and apical four-chamber view can easily see the liquid dark area is more evenly distributed in the periphery of the heart, it is more estimated than the M type The evolution of pericardial exudate volume is generally considered to be >8 mm in dark area and about 500 ml in volume; when the diameter is >25 mm, the amount of fluid is >1000 ml. Echocardiography may indicate the presence or absence of pericardial adhesion; the puncture site may be determined to guide pericardial puncture. It can be checked at the bedside.

3, X-ray inspection

X-ray examination has little value in the diagnosis of fibrinous pericarditis, and it has certain value for exudative pericarditis. When the pericardial effusion exceeds 250ml, the heart shadow may increase and the normal contour of the heart disappears. It is in the shape of a drop or a flask, and the heart shadow changes with the change of body position. Perspective or X-ray recording can show that the heart beats weakened or disappeared. If the X-ray film shows a clear lung field in a short period of time, the heart shadow increases rapidly. It is often an early and reliable clue for the diagnosis of pericardial effusion. X-ray films can also provide etiological diagnostic clues for tuberculous or neoplastic pericarditis. In addition, about 25% of patients with pericarditis have pleural effusion, and more On the left side, the pleural effusion in patients with heart failure is different on the right side.

4. Radionuclide inspection

When the pericardial effusion is examined by intravenous blood pool scanning after 99m intravenous injection, there is a blank area around the heart chamber, the heart shadow can be reduced or normal, the outer edge of the heart is irregular (especially the right edge is more common), scanning heart The ratio of the shadow transverse diameter to the X-ray heart shadow transverse diameter is less than 0.75.

5, magnetic resonance imaging

It can clearly show the volume and distribution of pericardial effusion, and can distinguish the nature of effusion. For example, non-hemorrhagic exudate is mostly low signal intensity; uremic, traumatic, tuberculous exudate contains more protein and cells , visible medium or high signal strength.

6, pericardial puncture

After clear pericardial effusion, feasible pericardial puncture for oozing, culture, cytology, etc., to help determine its nature or pathogen, pericardial effusion determination of adenosine deaminase (ADA) activity 30U / L is highly specific for the diagnosis of tuberculous pericarditis. After the pumping, air is injected into the pericardium (100-150ml) for X-ray film. The thickness of the pericardium can be understood. The medullary surface is regular (the tumor can cause localized bulge) , the size and shape of the heart, when a large number of pericardial effusion leads to cardiac tamponade, it is feasible to treat the pericardial puncture and decompression, or to inject the drug into the pericardial cavity for the cause.

7, fiber pericardoscopy

Anyone who has pericardial effusion requiring surgical drainage may have a fiber pericardial examination. The pericardium mirror observes the characteristics of pericardial lesions under direct vision of the light guide, and can perform a pericardial biopsy under the condition of clearing the lesion to improve the accuracy of etiological diagnosis. .

Diagnosis and diagnosis of acute pericarditis

diagnosis

The diagnosis of acute pericarditis can be diagnosed based on symptoms, signs, X-ray and echocardiography. The symptoms of chest pain and systemic reactions such as fever should be considered. If you hear the pericardial friction, the diagnosis is certain. However, pericardial friction sounds vary in length, so it should be observed repeatedly to avoid missed diagnosis. Patients with dyspnea, tachycardia, dilated heart and venous congestion, should think of pericardial effusion, X-ray and echocardiography Examination can generally establish a diagnosis.

Differential diagnosis

1, early repolarization syndrome: ST-T changes on the electrocardiogram can occur, and should be differentiated from ST-T changes on the electrocardiogram of acute pericarditis.

2, acute myocardial ischemia: acute pericarditis, chest pain due to chest pain in the posterior sternal or anterior region, can be radiated to the neck and back, sharp pain; easy to coronary atherosclerotic heart disease The clinical manifestations of acute myocardial ischemia such as angina pectoris and myocardial infarction are confused and attention is given to identification.

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