Pericarditis: general information

Pericarditis is an inflammation of the pericardium, often accompanied by accumulation of effusion in its cavity. Pericarditis can be caused by many causes (for example, infectious process, myocardial infarction, trauma, tumors, metabolic disorders), but it is often idiopathic. Symptoms include chest pain or a feeling of pressure, often worse with deep breathing. Cardiac output can be significantly reduced. Diagnosis is based on clinical manifestations, pericardial friction noise, changes in ECG data and the presence of effusion in the pericardial cavity according to X-ray or echocardiography. To determine the cause of pericarditis, further examinations are needed. Treatment depends on the cause of the disease, but common approaches include the use of analgesics, anti-inflammatory drugs and (sometimes) surgical intervention.

Pericarditis is the most frequent pathology of the pericardium. Congenital diseases of the pericardium are rare.

The pericardial syndrome can be caused by hemopericardium, the accumulation of exudate in the form of hydropericardium, more often the formation of pericarditis is noted. In all cases, emergency care is required in the conditions of a cardiac or cardiosurgical hospital, in intensive care units.

Pericarditis is a secondary pathology complicating the course of the underlying disease, most often the systemic one, which is characterized by the development of a polyserositis, more often involving the pleural cavity and joints in the process. No statistical data was found, as pericarditis is not always diagnosed. But pathology, most likely, is more frequent than it is customary to think. According to DG Lingkog (1996), signs of pericarditis are detected in 17.9% of autopsies. In women, pathology is observed 3 times more often than in men, which is especially pronounced in individuals under 40.

[1], [2], [3],

Anatomy and pathophysiology of the pericardium

Pericardium consists of two layers. The visceral layer of the pericardium consists of a single layer of mesothelial cells. It is attached to the myocardium, it can stretch in the places of passage of large vessels and connects with a dense fibrous layer enveloping the heart (the parietal layer of the pericardium). The cavity formed by these layers contains a small amount of liquid (<25-50 ml), consisting mainly of ultrafiltrate of plasma. Pericardium limits the extensibility of the heart chambers and increases the efficiency of cardiac contraction.

Pericardium is richly innervated by sympathetic and somatic afferent fibers. Tensile-sensitive mechanoreceptors respond to changes in cardiac volume and stretching of the organ walls, resulting in transient pericardial pain. The diaphragmatic nerve (n. Phrenicus) passes in the parietal pericardial sheet, so it is possible to damage it during surgery on the pericardium.

[4], [5], [6]

How is pericarditis manifested?

Pericarditis has polymorphic symptoms, they depend on the form and course of the underlying disease that caused its development.

Dry (fibrinous) pericarditis

It is characterized by chest pain and pericardial friction noise. It is often combined with fibrinous pleurisy. Pericarditis itself does not cause changes in hemodynamics, but pericardium is richly innervated, so many clinical manifestations are of a neuro-reflex character: palpitation, dyspnea, dry cough. The patient can not make a deep breath, movement and movement are painful. Typical localization of pain - behind the breastbone, but it can be irradiation under the left scapula, neck, xiphoid process, right half of the thorax.

In the physical examination, a painful reaction is observed when pressing on the reflex points of the heart: above the sternoclavicular joint on the left, in the middle part of the sternum handle, over the xiphoid process and under the left scapula. The noise of friction of the pericardium, revealed during auscultation, has a clear localization - it is heard only within the limits of absolute dullness and merges with the systolic murmur of the heart. Especially well it is audible at pressing a stethoscope, a throwing over of a head of the patient, an inclination forward. Depending on the etiology, there may be a rapid arrest of the process, within a few hours in viral diseases; transformation in the effusive, more often with rheumatism; to acquire a protracted character in auto-allergies, usually with the transition to fibrotic.

[7], [8], [9], [10], [11]

Pericardial effusion

It is accompanied by a brighter clinical picture, although it is also not always diagnosed, as the clinical manifestations depend on the nature; effusion, its volume, and most importantly - the rate of accumulation-exudate. With a slow accumulation of exudate, the pericardium gradually stretches, without causing disturbances in hemodynamics, even with the accumulation of 2-3 liters of fluid. Only an increase in intrapericardial pressure of more than 300 mm. Water. Art. Leads to the development of symptoms of cardiac tamponade. Intrapericardial pressure is determined according to CVP, it exceeds it by 20-30 mm. Water. Art. With rapid accumulation of exudate, CVP does not significantly increase, and cardiac arrest occurs from reflex disorders, already with the accumulation of fluid above 200-500 ml.

With a slow accumulation of exudate, the friction noise of the pericardium gradually disappears, the apical impulse shifts up and to the right (Jandren's symptom). Percussion symptoms change dramatically. The borders of the heart expand considerably in all directions, especially to the right, sometimes reaching the middle-clavicular line (the symptom of Rothch): on the right, when the cardiac dullness changes to the hepatic, a straight line is formed, but an obtuse angle (Ebstein's symptom). In the epigastrium, swelling is noted, percussion dullness occupies the entire epigastrium - the Taube space (Auenbrug-tepa symptom). Absolute stupidity is very clear "woody"), merges with the relative area, and above it a very bright tympanitis (the symptom of Edlefsen-Poten). With a large sweat under the left shoulder blade, absolute stupidity is revealed percussionally, and bronchial breathing is performed during auscultation, which is associated with the lungs contracting the pericardial effusion (Bamberger symptom). The auscultatory picture is poorly expressed: weakening of heart sounds; noise pericardium friction in the normal position of the patient is audible, but it appears when you roll your head and inhale with a delay in breathing (a symptom of Gerke).

With exudative pericarditis, cardiac tamponade develops rarely, more often the process passes into the adhesive and fibrous forms. As the resorption of the exudate and the formation of adhesive or fibrous pericarditis, symptoms of compression appear. Respiratory excursions of the anterior thoracic region decrease (Williams symptom). The stomach stops participating in the act of breathing (Minter's symptom). There is a "barking" cough (Shchagumovich's symptom). The swallowing act is broken, and the voice changes up to aphonia.

Signs of the development of cardiac tamponade are: a decrease in blood pressure, pulse filling, the development of tachycardia and arrhythmias, mainly of tachycystolic forms. CVP rises more than 20 mm of water. Art. Filling of the pulse is associated with breathing - at the height of the inspiration the filling decreases (Kussmaul's symptom). Characterized by the type of patient: cyanosis, face and neck swelling, forming the symptoms of the "consular head" of the "Stokes collar," the cervical and peripheral veins swell, but neck neck pulsation is absent, and their filling increases. Because of the compression of the superior vena cava, which leads to edema of the liver and the development of ascites, the patient takes a forced position to discharge it: sitting, the body tilted forward with a forehead resting on the pillow (Breitman's pose), or standing on all fours, leaning on the pillow with his forehead and shoulders.

Purulent pericarditis

Primarily rarely develops, more often there is an attachment of microflora and suppuration against the background of the exudative process. Therefore, their clinical manifestations are the same. A distinctive feature is the development of purulent-resorptive fever, and then a syndrome of purulent intoxication. Purulent pericarditis, as a rule, results in the formation of an adhesive or fibrous pericarditis, which sometimes requires pericardectomy.

Classification of pericarditis

Classification of pericarditis is limited to etiology and clinical and morphological manifestations. According to etiology, pericarditis is divided into: non-infectious, developing with systemic diseases (rheumatism, lupus erythematosus, tuberculosis, etc.), as an autoallergic process after myocardial infarction, chest trauma, as manifestations of pulmonary hypertension, metabolic diseases, etc., purulent, developing with direct hit the microflora in the pericardium. In the International Statistical Classification, more attention is paid to rheumatism, as the main reason for the development of pericarditis, it is divided into: rheumatoid, acute non-rheumatoid, and other pericardial lesions. According to the clinical course, pericarditis is divided into acute and chronic. According to clinical and morphological manifestations, pericarditis is divided into: fibrinous (dry), exudative (serous, serous-hemorrhagic, serous-fibrinous exudate), purulent, adhesive (adherent), fibrous (cicatricial).

Pericarditis is acute and chronic. Acute pericarditis develops rapidly, accompanied by an inflammatory reaction. Chronic pericarditis (existing more than 6 months) develops more slowly, its important characteristic is effusion.

Acute pericarditis can go to chronic. Unfavorable hemodynamic changes and rhythm disturbances are rare, although there is sometimes a cardiac tamponade. In some cases with pericardial develops a pronounced thickening and pericardial tension (constrictive pericarditis). Pericarditis can lead to inflammation of the epicardial part of the myocardium.

Pericardial effusion is the accumulation of fluid in the pericardial cavity. The fluid can be serous (sometimes with fibers of fibrin), serous-hemorrhagic, chyleous, with blood or pus.

Cardiac tamponade occurs when a large amount of effusion in the pericardium interferes with the filling of the heart with blood, leading to a low cardiac output, sometimes shock and death. If the liquid (usually blood) accumulates quickly, even a small amount (for example, 150 ml) can lead to a tamponade, since the pericardium can not stretch quickly enough to adapt to such conditions. Slow accumulation of even 1500 ml may not lead to tamponade. Localized fluid accumulation can cause a limited tamponade of the right or left side of the heart.

Constrictive pericarditis, which rarely occurs, is a consequence of the extensive inflammatory fibrous thickening of the pericardium. Sometimes the visceral and parietal layers are glued together or with the myocardium. Fibrous tissue often contains calcium deposits. The severe thickened pericardium significantly impairs the filling of the ventricles, reducing the shock volume and cardiac output. Significant accumulation of fluid in the pericardium occurs rarely. Violations of rhythm often occur. The diastolic pressure in the ventricles, atria and the venous vessels that enter the heart becomes virtually the same. A systemic venous congestion arises, causing considerable sweating of the liquid from the capillaries, with the development of edema and (later) ascites. Chronic increase in systemic venous and hepatic venous pressure can lead to cardiac cirrhosis of the liver.

[12], [13], [14], [15], [16], [17], [18], [19],