Pericarditis: general information

Pericarditis is an inflammation of the pericardium, often accompanied by accumulation of effusion within its cavity. Pericarditis may have many causes (eg, infection, myocardial infarction, trauma, tumors, metabolic disorders), but is often idiopathic. Symptoms include chest pain or pressure, often aggravated by deep breathing. Cardiac output may be significantly reduced. Diagnosis is based on clinical manifestations, pericardial friction rub, ECG changes, and the presence of pericardial effusion on radiography or echocardiography. Further investigation is needed to identify the cause of pericarditis. Treatment depends on the cause, but general approaches include analgesics, anti-inflammatory drugs, and (sometimes) surgery.

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

Pericardial syndrome can be caused by hemopericardium, accumulation of exudate in the form of hydropericardium, but more often the formation of pericarditis is observed. In all cases, emergency care is required in a cardiology or cardiac surgery hospital, in intensive care units.

Pericarditis is a secondary pathology that complicates the course of the underlying disease, most often systemic, characterized by the development of polyserositis, often with the involvement of the pleural cavity and joints. No statistical data have been found, since pericarditis is not always diagnosed. But the pathology is most likely more common than is commonly thought. According to DG Lingkog (1996), signs of past pericarditis are detected in 17.9% of autopsies. In women, the pathology is observed 3 times more often than in men, which is especially pronounced in people under 40 years of age.

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Anatomy and pathophysiology of the pericardium

The pericardium consists of two layers. The visceral layer of the pericardium consists of a single layer of mesothelial cells. It is adjacent to the myocardium, can stretch where large vessels pass, and is connected to a dense fibrous layer that envelops the heart (parietal layer of the pericardium). The cavity formed by these layers contains a small amount of fluid (<25-50 ml), consisting mainly of plasma ultrafiltrate. The pericardium limits the distensibility of the cardiac chambers and increases the efficiency of cardiac contraction.

The pericardium is richly innervated by sympathetic and somatic afferent fibers. Stretch-sensitive mechanoreceptors respond to changes in cardiac volume and stretching of the organ walls, which can cause transient pericardial pain. The phrenic nerve (n. Phrenicus) passes through the parietal layer of the pericardium, so it can be damaged during surgery on the pericardium.

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How does pericarditis manifest itself?

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

Dry (fibrinous) pericarditis

Characterized by chest pain and pericardial friction rub. Often combined with fibrinous pleurisy. Pericarditis itself does not cause changes in hemodynamics, but the pericardium is richly innervated, so many clinical manifestations are of a neuroreflex nature: palpitations, shortness of breath, dry cough. The patient cannot take a deep breath, movements and displacements are painful. The localization of pain is characteristic - behind the sternum, but it can radiate under the left shoulder blade, to the neck, xiphoid process, right half of the chest.

During physical examination, a painful reaction is noted when pressing on the reflex points of the heart: above the sternoclavicular joint on the left, in the middle part of the manubrium of the sternum, above the xiphoid process and under the left scapula. The noise of pericardial friction, revealed during auscultation, has a clear localization - it is heard only within the limits of absolute dullness and merges with the systolic heart murmur. It is especially well heard when pressing with a stethoscope, throwing back the patient's head, bending forward. Depending on the etiology, there may be a rapid relief of the process, in a few hours in viral diseases; transformation into exudative, more often in rheumatism; acquire a protracted nature in autoallergies, usually with a transition to fibrous.

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Pericarditis with effusion

It is accompanied by a more vivid clinical picture, although it is also not always diagnosed, since clinical manifestations depend on the nature of the effusion, its volume, and most importantly - on the rate of accumulation of exudate. With a slow accumulation of exudate, the pericardium gradually stretches, without causing hemodynamic disturbances, even with an accumulation of 2-3 liters of fluid. Only an increase in intrapericardial pressure over 300 mm H2O leads to the development of symptoms of cardiac tamponade. Intrapericardial pressure is determined by the central venous pressure, it exceeds it by 20-30 mm H2O. With rapid accumulation of exudate, the central venous pressure does not increase significantly, and cardiac arrest occurs from reflex disturbances, already with an accumulation of fluid over 200-500 ml.

With a slow accumulation of exudate, the pericardial friction noise gradually disappears, the apical impulse shifts upward and to the right (Jandren's symptom). Percussion symptoms change significantly. The borders of the heart expand significantly in all directions, especially to the right, sometimes reaching the midclavicular line (Rotch's symptom): on the right, when cardiac dullness passes into hepatic dullness, an obtuse angle is formed instead of a right one (Ebstein's symptom). A bulge is noted in the epigastrium, percussion dullness occupies the entire epigastrium - Taube's space (Auenbrugger's symptom). Absolute dullness is very clear "woody"), merges with the relative area, and above it there is very bright tympanitis (Edlefsen-Poten's symptom). With a large effusion under the left scapula, percussion reveals absolute dullness, and auscultation reveals bronchial breathing, which is associated with compression of the lung by pericardial effusion (Bamberger's symptom). The auscultatory picture is weakly expressed: weakening of heart tones; pericardial friction noise is heard in the patient's normal position, but it appears when throwing the head back and during inhalation with breath holding (Gerke's symptom).

In exudative pericarditis, cardiac tamponade rarely develops; more often, the process develops into adhesive and fibrous forms. As the exudate is absorbed and adhesive or fibrous pericarditis is formed, symptoms of compression appear. Respiratory excursions of the anterior chest decrease (Williams' symptom). The abdomen stops participating in the act of breathing (Minter's symptom). A "barking" cough appears (Shchagumovich's symptom). The act of swallowing is impaired, and the voice changes to the point of aphonia.

Signs of cardiac tamponade development are: decreased blood pressure, pulse filling, development of tachycardia and arrhythmia, mainly tachystolic forms. CVP increases by more than 20 mm H2O. Pulse filling is associated with breathing - at the height of inspiration, filling decreases (Kussmaul symptom). The patient's appearance is characteristic: cyanosis increases, swelling of the face and neck, forming the symptoms of "consular head" "Stokes collar", the cervical and peripheral veins swell, but there is no pulsation of the veins of the neck, on inspiration their filling increases. Due to compression of the superior vena cava, which leads to liver edema and the development of ascites, the patient takes a forced position to unload it: sits, the body is tilted forward, the forehead rests on a pillow (Breitman pose) or gets on all fours, leaning his forehead and shoulders on the pillow.

Purulent pericarditis

Primary development is rare, more often there is the addition 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 purulent intoxication syndrome. Purulent pericarditis, as a rule, ends with the formation of adhesive or fibrous pericarditis, which sometimes requires pericardiectomy.

Classification of pericarditis

The classification of pericarditis is limited by etiology and clinical and morphological manifestations. By 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 penetration of microflora into the pericardium. In the International Statistical Classification, more attention is paid to rheumatism as the main cause of pericarditis, it is divided into: rheumatoid, acute non-rheumatoid, other lesions of the pericardium. 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 (sticky), fibrous (scarring).

Pericarditis can be acute or chronic. Acute pericarditis develops quickly, accompanied by an inflammatory reaction. Chronic pericarditis (existing for more than 6 months) develops more slowly, its important characteristic is effusion.

Acute pericarditis may become chronic. Adverse hemodynamic changes and rhythm disturbances are rare, although cardiac tamponade sometimes occurs. In some cases, pericarditis develops marked thickening and tension of the pericardium (constrictive pericarditis). Pericarditis may lead to inflammation of the epicardial part of the myocardium.

Pericardial effusion is an accumulation of fluid in the pericardial cavity. The fluid may be serous (sometimes with fibrin threads), serous-hemorrhagic, chylous, with blood or pus.

Cardiac tamponade occurs when a large amount of pericardial effusion prevents the heart from filling with blood, leading to low cardiac output, sometimes shock, and death. If fluid (usually blood) accumulates rapidly, even a small amount (eg, 150 mL) may cause tamponade because the pericardium cannot stretch quickly enough to accommodate these conditions. A slow accumulation of even 1500 mL may not cause tamponade. Localized fluid accumulation may cause limited tamponade of the right or left side of the heart.

Constrictive pericarditis, which is quite rare, is a consequence of extensive inflammatory fibrous thickening of the pericardium. Sometimes the visceral and parietal layers adhere to each other or to the myocardium. The fibrous tissue often contains calcium deposits. The rigid, thickened pericardium significantly impairs ventricular filling, reducing stroke volume and cardiac output. Significant accumulation of fluid in the pericardium is rare. Rhythm disturbances often occur. The diastolic pressure in the ventricles, atria, and venous vessels flowing into the heart becomes virtually identical. Systemic venous congestion occurs, causing significant fluid leakage 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.

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