Acute pericarditis

Acute pericarditis is an acute inflammation of the visceral and parietal pericardial sheets (both with pericardial effusion and without it) of various etiologies. Acute pericarditis can be an independent disease or a manifestation of systemic disease.

ICD-10 code

• 130. Acute pericarditis.

An acute pericardial effusion is included.

• 130.0. Acute nonspecific idiopathic pericarditis.
• 130.1. Infectious pericarditis.
• 130.8. Other forms of acute pericarditis.
• 130.9. Acute pericarditis, unspecified.

Epidemiology of acute pericarditis

The incidence of acute pericarditis is difficult to assess, since in many cases the disease is not diagnosed. The incidence of acute pericarditis among hospitalized patients is about 0.1%. The disease can occur at any age.

[1], [2], [3], [4], [5]

Causes of acute pericarditis

About 90% of cases of isolated acute pericarditis have a viral or unknown etiology. Idiopathic acute pericarditis is diagnosed if a specific etiology is not established with a completely completed standard examination. There are no clinical differences between idiopathic cases and viral pericarditis (probably most idiopathic cases are diagnosed viral infections).

Typical in the past, the causes of acute pericarditis (tuberculosis or bacterial infection) have now become rare. Bacterial infections cause acute purulent pericarditis by direct spread of lung infection, with penetrating chest injuries, sub-diaphragmatic abscess, or as a result of hematogenous infection with myocardial abscesses or infective endocarditis. Tuberculosis should be considered in cases of acute pericarditis without rapid flow, especially in groups of patients at high risk of tuberculosis.

Acute pericarditis can occur in patients with myocardial infarction; most often it develops 1-3 days after transmural infarction (presumably due to the effect of necrotic myocardium on the adjacent pericardium); the second form of acute pericarditis associated with myocardial infarction - dressler's syndrome - typically occurs in weeks or months after myocardial infarction. Acute pericarditis can develop after traumatic heart damage, surgery on the pericardium, or after a heart attack. Postcardiothyroid syndrome, like Dressler's syndrome, is presumed to be autoimmune in nature and occurs with signs of systemic inflammation, including fever and polyserositis. The incidence of pericarditis in myocardial infarction is reduced after reperfusion treatment.

Acute pericarditis is also observed in patients with uremia who need hemodialysis, with rheumatic fever, SLE, rheumatoid arthritis and other rheumatic diseases. A high incidence of acute pericarditis was noted during irradiation of the thorax and mediastinum.

[6]

Pathogenesis of acute pericarditis

All the symptoms of uncomplicated acute pericarditis are due to inflammation of the pericardium. Increased vascular permeability in inflammation leads to exudation of the liquid fractions of the blood, fibrinogen, which is deposited as fibrin into the pericardial cavity and forms a catarrhal and then fibrinous (dry) pericarditis. With extensive involvement of the pericardium in inflammation, exudation of liquid fractions of blood exceeds reabsorption, which leads to the formation of pericardial effusion (exudative pericarditis). Depending on the etiology of acute pericarditis effusion can be serous, serous-fibrinous, hemorrhagic, purulent, putrefactive. The volume of a large pericardial effusion can reach a liter or more (normal in the pericardial cavity contains 15-35 ml of serous fluid). Rapid accumulation of even a small amount of it can lead to an increase in pressure in the pericardial cavity. The resulting infringement of filling the right cavities of the heart leads to a compensatory increase in systemic venous pressure. If the pressure in the pericardial cavity becomes equal to or higher than the filling pressure of the right heart cavities, a cardiac tamponade develops with the collapse of the right atrium and ventricle in the diastole and a drop in cardiac output and systemic BP. Approximately 15% of patients have acute pericarditis combined with myocarditis.

Symptoms of acute pericarditis

The diagnosis of "acute pericarditis" is usually given to patients with a characteristic triad:

• auscultation of pericardial friction noise;
• chest pain;
• typical sequential changes in the ECG.

Further examination is aimed at assessing the presence of pericardial effusion and hemodynamic disorders, as well as determining the cause of the disease.

Anamnesis and complaints of patients

Most patients with acute pericarditis (90%) experience chest pain:

• the pain is localized behind the sternum with spread to the neck, left shoulder, arms, trapezius muscles; children experience epigastric pain;
• the onset of pain can be sudden, then the pain becomes permanent (lasting for hours and days), often monotonous, can be acute, blunt, with burning or pressure;
• The intensity of pain can range from mild to severe;
• pain usually increases with inspiration, lying on the back, during swallowing, or when the body moves, decreases in a sitting position directly or with a forward inclination;
• in some cases, pain in the heart may be absent, for example, it is often observed with pericarditis in patients with rheumatoid arthritis.

When studying the anamnesis of the disease in patients, a connection can be found between the occurrence of pain in the heart and infection; in the prodromal period, fever, weakness, myalgia can be observed. Information on tuberculosis, autoimmune or tumor diseases in the past can help in the diagnosis of specific causes of acute pericarditis.

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

Clinical symptoms that allow suspected pericardial effusion

Complaints of the patient.

• The feeling of compression, discomfort in the chest.
• Palpitation.
• Persistent dry "barking" cough, shortness of breath, hoarseness of voice.
• Hiccough, dysphagia.

Physical examination.

• The cardiovascular system
  • Expansion of cardiac dullness in all directions, change in heart boundaries when the position changes (in the standing position, the zone of dullness in the second and third intercostal spaces is shortened, and in the lower divisions widens), the unusual intensity of dullness of the heart, the coincidence of the zone of absolute stupidity of the heart with the zone of relative dullness in the lower divisions .
  • The displacement of the apical impulse upwards and downwards from the lower boundary of the stupidity of the heart (the sign of Jardin), the apical impulse is weakened.
  • Swelling of the cervical veins, an increase in central venous pressure.
  • The heart sounds are sharply weakened in the lower left parts of the dullness of the heart, but can be heard well from within the apical impulse.
  • If there is a pericardial friction noise, then it is better heard in the prone position at the end of the inspiration (Poten's symptom) or when the head is rolled back (the Herks symptom), with an increase in the effusion the noise may disappear.
  • Tachycardia (may be absent in hypothyroidism or uremia).
  • Acrocyanosis. 
• Respiratory system
  • Sign of Edward - blunt percussion sound below the angle of the left scapula due to compression of the left lung with pericardial effusion, in this place voice tremor is strengthened, breathing is weakened. When tilted forward, dullness under the scapula disappears, but small bubbling rales (Pen's sign) appear.
• System of the digestive system
  • The abdomen does not participate in the act of breathing (Winter's sign) due to the limitation of the diaphragm's mobility.
  • Small or slowly accumulating pericardial effusions can be asymptomatic. Large effusions are observed in no more than 5% of cases of acute pericarditis. Unrecognized pericardial effusion can lead to a rapid, unexpected deterioration in the condition and death of the patient from the cardiac tamponade.

[12], [13], [14]

Complications of acute pericarditis

• cardiac tamponade;
• relapses of acute pericarditis occur in 15-32% of patients; more often with autoimmune pericarditis, some cases of relapse may be associated with reactivation of viral pericarditis or inadequate treatment in the first episode of acute pericarditis. Relapses occur more often after treatment with glucocorticoids, pericardiotomy or pericardial window creation, less often after colchicine treatment; relapses can be repeated for several years spontaneously or when discontinuing the use of anti-inflammatory drugs;
• chronic constructive pericarditis in outcome (less than 10%).

Idiopathic or viral acute pericarditis is rarely complicated by cardiac tamponade. To situations with threat, cardiac tamponades include a moderate or large fresh or increasing effusion, purulent acute pericarditis, tuberculous acute pericarditis, bleeding into the pericardial cavity. The greatest risk of progression of pericardial effusion to tamponade is in patients with a recently developed large pericardial effusion with signs of diastolic collapse of the right heart. Although the probability of tamponade is small (according to transthoracic echocardioma), the probability of tamponade is low, it can occur unexpectedly in case of fast fluid accumulation, for example in hemopericardium, or if in fact there is a large but unusually located effusion that is not recognized in transthoracic echocardiography, and also some cases of a combination of a large pleural and a small pericardial effusion. Therefore, it is necessary to suspect tamponade in cases of disorders in patients with hemodynamics, regardless of the amount of pericardial fluid. Cardiac tamponade can occur sharply abruptly or be observed for a long time. The clinical symptomatology of cardiac tamponade depends on the degree of increase in pericardial pressure: with a slight increase in pressure (<10 mm Hg) tamponade is often asymptomatic, with moderate and especially with a sharp increase in pressure (> 15 and up to 20 mm Hg) a feeling of discomfort in the heart and there is shortness of breath. Clinical and instrumental diagnostics of tamponades are presented below. If there is a suspicion of cardiac tamponade, an urgent echocardiographic study is indicated.

[15]

Clinical symptoms indicative of cardiac tamponade or its threat in acute pericarditis

Complaints of the patient:

• the appearance of agonizing attacks of severe weakness with a weak frequent pulse;
• the appearance of fainting, dizziness, fear of death;
• increased dyspnea (due to hypovolemia of the small circle of blood circulation).

Inspection data and physical research methods:

The cardiovascular system:

• swelling of the cervical veins (less noticeable in patients with hypovolaemia); high indices of central venous pressure (200-300 mmW), with the exception of cases of tamponade at low pressure in patients with hypovolemia; decrease in venous pressure on inspiration persists;
• arterial hypotension (may be absent, especially in patients with previously observed arterial hypertension);
• Bek's triad with pericardial tamponade: arterial hypotension, weakening of cardiac tones, expansion of jugular veins;
• paradoxical pulse: a decrease in systolic blood pressure by more than 10 mm Hg. When inhaled;
• increasing tachycardia;
• weak peripheral pulse, weakened by inspiration;
• pronounced acrocyanosis. 

Respiratory system: 

• shortness of breath or rapid breathing in the absence of wheezing in the lungs.

System of the digestive system:

• increase and soreness of the liver;
• appearance of ascites.

General inspection:

• the patient's position sitting with an inclination forward and forehead resting on the pillow (Breitman's pose), a posture of a deep bow;
• pallor of the skin, gray cyanosis, cold extremities;
• there may be swelling of the face, swelling of the shoulder and arm, more left (compression of an unnamed vein);
• growth of peripheral edema.

In the most severe cases, patients may lose consciousness and, with the exception of an increase in venous pressure, the clinical picture resembles hypovolemic shock. An imperceptibly developing cardiac tamponade can debut with symptoms of complications associated with impaired blood circulation in the organs - renal failure, shock liver, mesenteric ischemia. Cardiac tamponade in a patient with fever can be mistakenly regarded as a septic shock.

[16], [17], [18], [19], [20]

The technique of determining the paradoxical pulse

The cuff is injected to a pressure higher than the systolic pressure. With a slow descent of air listening intermittent tone Korotkov. Comparing with the patient's breathing cycle, establish a point at which the tone is heard on exhalation and disappears on inspiration. With further decrease in pressure in the cuff, a point is reached at which the tone is heard throughout the entire breathing cycle. The difference in systolic pressure between these points is more than 10 mm Hg. Is defined as a positive paradoxical pulse. For rapid clinical orientation, this feature can also be examined by simple palpation of the pulse on the radial artery, which significantly decreases or disappears during normal shallow inspiration. Paradoxical pulse is not pathognomonic symptom of cardiac tamponade and can also be observed with pulmonary embolism, subacute mitral regurgitation, right ventricular infarction, bronchial asthma. On the other hand, the paradoxical pulse is difficult to detect in patients with cardiac tamponade in severe shock, it may also be absent in cardiac tamponade in patients with concomitant pathological changes in the heart: aortic valve insufficiency, interatrial septal defect, hypertrophy or left ventricular dilatation,

Instrumental methods for diagnosis of cardiac tamponade (Guidelines for diagnosis and treatment of pericardial diseases of the European Society of Cardiology, 2004)

Method of research	Results of the study with cardiac tamponade
ECG	May be normal or have nonspecific changes (ST-T prong); electrical alteration (variability of QRS voltage, less often of T wave, caused by excessive cardiac mobility), bradycardia (in the late stage); electromechanical dissociation (in the atonal phase)
Chest X-ray	Increased heart shadow with normal pulmonary pattern
Echocardiography	A large "circular" pericardial effusion: a late diastolic collapse of the right atrium (the most sensitive symptom is observed in 100% of patients with cardiac tamponade), an early diastolic collapse of the anterior free wall of the right ventricle; collapse of the right ventricle, continuing more than a third of the diastole (the most specific symptom); collapse of the left atrial wall at the end of diastole and the beginning of systole (observed in approximately 25% of patients with tamponade has high specificity); an increase in the thickness of the walls of the left ventricle in the diastole, pseudohypertrophy "; dipatazin lower vena cava, a decrease in the collapse of the inferior vena cava on inspiration (less than 50%); "A swaying heart"
Echocardiography	Strengthening the tricuspid flow and mitral flow reduction during inspiration (with exhalation reversed); Systemic veins reduced systolic and diastolic flow on exhalation and increased backflow with atrial contraction
Color Doppler echocardiography	Significant fluctuations of mitral and tricuspidal flow associated with respiration
Cardiac catheterization	Confirmation of the diagnosis and quantitative assessment of hemodynamic disorders; pressure in the right atrium is increased by 10-30 mm Hg, (systolic X-fold is retained and diastolic Y-recession of the right atrial pressure curve and systemic venous pressure is absent or reduced); the pressure in the pericardial cavity is increased and almost equal to the pressure in the right atrium (both pressures decrease with a zdoh): the mean diastolic pressure in the right ventricle is increased and equal to the right atrial pressure and pericardial cavity pressure (without "diastolic sinking and plateau"); diastolic pressure in the pulmonary artery slightly elevated and can correspond to pressure in the right ventricle - pulmonary capillary wedge pressure is also increased and almost equal to the pressure in the pericardial cavity and pressure in the right atrium: systolic pressure in the left ventricle and aorta can be normal or reduced Confirm that aspiration pericardial effusion leads to improved hemodynamics Detection of concomitant hemodynamic disorders (left ventricular failure, constriction, pulmonary hypertension ziya)
Angiography of the right and left ventricles	Atrial collapse and small hyperactive cavities of the ventricles
Computed tomography	Change in the configuration of the ventricles and atria (atrial and ventricular collapse)

Example of the formulation of the diagnosis

Acute idiopathic pericarditis. HK0 (1 FC).

[21], [22], [23], [24],

Differential diagnosis of acute pericarditis

Differential diagnosis is carried out with other diseases, which are characterized by pain behind the breastbone. First of all, life-threatening causes of pain and heart such as myocardial infarction, aortic dissection, pulmonary embolism, angina pectoris are excluded. The plan for differential diagnosis also includes pleurisy or pleuropneumonia, spontaneous pneumothorax, herpes zoster, esophagitis, esophagospasm, esophagus rupture, in some cases acute gastritis and stomach ulcer, traumatic diaphragmatic hernia, Tietze syndrome and some other diseases that cause chest pain . The noise of friction of the pericardium should be differentiated with a pleural friction noise, the latter disappears with a delay in breathing, while the pericardial friction noise with respiratory arrest is preserved.

Changes in the electrocardiogram with acute pericarditis are similar to changes in myocardial infarction, the syndrome of early repolarization, and the Brugada syndrome. Nevertheless, with myocardial infarction, SD elevation is domed, focal changes with reciprocal depression of the ST segment, and not diffuse, as in acute pericardial (with postinfarction pericardial ST elevation segment may also be localized); characterized by the formation of pathological Q and a decrease in the voltage of the R-wave, negative T appear before the normalization of ST, the PR depression is atypical. In the syndrome of early repolarization, elevation of the ST segment is observed in fewer leads. There is no depression of the PR segment and ST-T stage changes. In the Brugada syndrome, the rise of the ST segment is limited to the right thoracic leads (VI-VZ) against the background of changes in the QRS complex. Similar to the blockade of the right leg of the bundle.

With pericardial swelling differential diagnosis is performed with effusions of non-inflammatory nature (with heart failure, nephrotic syndrome, hypothyroidism).

Clinical signs of cardiac tamponade differentiate with other urgent conditions that cause arterial hypotension, shock and increased systemic venous pressure, including cardiogenic shock in myocardial diseases, myocardial infarction of the right ventricle, acute right ventricular failure due to pulmonary embolism or other causes. When evaluating the results of echocardiography in a patient with suspected cardiac tamponade, one should keep in mind that the diastolic collapse of the right atrium, characteristic of cardiac tamponade, can be caused by massive pleural effusion.

For the diagnosis of concomitant myocarditis in patients with acute pericarditis, the following symptoms are important:

• unexplained weakness and fatigue during exercise, palpitations,
• arrhythmias, especially ventricular arrhythmias;
• echocardiographic signs of myocardial dysfunction;
• Elevation of the ST segment at the onset of the disease;
• increased level of troponin I for more than 2 weeks, CK and myoglobin.

[25], [26], [27], [28], [29], [30]

Diagnosis of acute pericarditis

The pathognomonic sign of acute pericarditis is the pericardial friction noise, which is determined in 85% of patients with this disease:

• noise scratching, scraping, such as rubbing the skin against the skin;
• Typical noise (more than 50% of cases) has three phases:
  • 1-st phase - presystolic murmur preceding I tone, which occurs during atrial systole;
  • 2 nd phase - systolic murmur between I and II tone, which occurs in the systole of the ventricles and coincides with the peak of the pulse on the carotid arteries;
  • 3rd phase - early diastolic murmur after II tone (usually the weakest), reflects the rapid filling of the ventricles in early diastole;
• with tachycardia, atrial fibrillation or at the onset of the disease, the noise may be a two-phase systolic-diastolic or monophasic systolic;
• noise is better heard over the left lower edge of the sternum within the limits of absolute stupidity of the heart and is not carried out anywhere;
• noise is variable in time, is weaker heard at the beginning of the disease. In order not to miss it, frequent repeated auscultation is necessary;
• can persist even with the appearance of pericardial effusion.

Often patients have subfebrile temperature; but fever above 38 C with chills is unusual and may indicate the likelihood of purulent bacterial acute pericarditis. In accordance with the etiology, there may be other signs of a general or systemic disease. The rhythm of the heart with acute pericardial is usually correct, but often there is a tachycardia. Breathing can be superficial because of pain; shortness of breath is possible.

In the presence of pericardial effusion, there are symptoms due to an increase in the volume of the pericardial sac, a violation of the venous flask, a decrease in cardiac output.

[31], [32], [33], [34], [35], [36], [37]

Instrumental and laboratory diagnostics of acute pericarditis

Changes ECG - the third classic diagnostic sign of acute pericarditis (occurs in 90% of patients). Typical ECG changes consistently go through 4 stages.

• In the early stage of acute pericarditis, the elevation of the ST segment with positive T-waves is typical for all leads except the leads aVR and VI, and the segment of the PR segment in the direction opposite to the P-wave. In some cases, the depression of the PR segment is observed in the absence of ST segment elevation.
• A few days later, the ST segment, and then the PR, return to the contour line
• Teeth T progressively flattened and inverted in most leads.
• The ECG usually returns to its original state after 2 weeks.
• In patients with uremic pericarditis, typical ECG changes may be absent. With pericardial effusion, low ECG voltage and sinus tachycardia are characteristic.

Transthoracic echocardiogram is the standard for non-invasive diagnosis of pericardial effusion. It must be done by all patients with acute pericarditis or with suspected disease. With echocardiography in patients with acute pericarditis, pericardial effusion can be detected, the sign of which is the echoesfree space between the visceral and the parietal pericardium. Small effusions are represented by an echo-free space of less than 5 mm and are visible on the back of the heart. With moderate effusions, the thickness of the echo-free space is 5-10 mm. Large effusions have a thickness of more than 1 cm and completely surround the heart. The presence of effusion confirms the diagnosis of acute pericarditis, but in most patients with dry acute pericarditis the echocardiogram is normal. Echocardiography allows to establish hemodynamic disorders caused by the development of cardiac tamponade, thus characterizing the importance of effusion, as well as evaluating the function of the myocardium, which is important for the diagnosis of concomitant myocarditis. Transesophageal echocardiography is useful for characterizing local effusions, pericardial thickening, and pericardial tumor lesions.

Chest X-rays are performed to assess the shadow of the heart, exclude changes in the lungs and mediastinum, which may indicate a specific etiology of pericarditis. With a dry acute pericardial heart shadow is not changed .. With a significant pericardial swelling (more than 250 ml), there is an increase and change in the configuration of the shadow of the heart ("flask shadow", spherical shape with acute large swelling, triangular shape with long existing effusions), weakening of the pulsation of the contour shadows of the heart.

Laboratory blood tests (general analysis, biochemical analysis):

• patients with acute pericarditis usually have signs of systemic inflammation, including leukocytosis, an increase in ESR and an increase in the level of C-reactive protein;
• a slightly elevated level of troponin I is observed in 27-50% of patients with viral or idiopathic pericarditis without other signs of myocardial damage. The level of troponin normalized within 1-2 weeks, a longer increase indicates a myopericarditis, which worsens the prognosis; an increase in the level of CK in acute pericarditis is observed less often;
• Creatinine and urea plasma increased sharply with uremic acute pericarditis;
• test for HIV infection.

Additional studies with acute pericarditis

Additional laboratory blood tests according to clinical indications:

• bacteriological examination (seeding) of blood in case of suspected purulent acute pericarditis;
• antistreptolysin-O titer for suspected rheumatic fever (in young patients);
• rheumatoid factor, antinuclear antibodies, antibodies to DNA, especially if the disease is prolonged or severe with systemic manifestations;
• evaluation of the function of the styloid gland in patients with a large pericardial effusion (suspected hypothyroidism):
• Special studies on cardiotropic viruses, as a rule, are not shown, since their results do not change the tactics of treatment.

Exercise of tuberculin test, sputum examination for mycobacterium tuberculosis, if the disease continues more than a pedeli.

Pericardiocentesis is indicated for cardiac tamponade or suspected purulent, tuberculous or tumorous exudative acute pericarditis. The clinical and diagnostic efficacy of routine drainage of large pericardial effusion (more than 20 mm in diastole fed by echocardiography is not shown.Pericardiocentesis is not indicated if a diagnosis can be made without this study or if the effusion in typical viral or idiopathic acute pericarditis resolves due to anti-inflammatory treatment, pericardiocentesis is contraindicated in case of suspicion of exfoliating aortic aneurysm, with uncorrected coagulopathy, anticoagulant treatment (if planned ardiotseptezu patients continuously receiving anticoagulants inside, should reduce INR <1.5), thrombocytopenia less than 50x10 ⁹ / L.

The analysis of the pericardial fluid should include examination of the cell composition (leukocytes, tumor cells), protein, LDH, adenosine deaminase (marker of cell-mediated immune response to tuberculosis mycobacterium, including activation of T-lymphocytes and macrophages), seeding, direct examination and PCR diagnostics on mycobacterium tuberculosis, special studies of pericardial fluid in accordance with clinical data (oncomarkers for suspected malignant disease, PCR diagnostics for cardiotropic viruses In case of suspicion of viral pericarditis, the "milk" type of effusion is examined for triglycerides).

Computed tomography, magnetic resonance imaging can detect small and localized pericardial effusions that can be missed in Echocardiography, characterize the composition of the pericardial fluid and can be useful with conflicting results from other imaging studies.

If the expressed clinical activity persists for 3 weeks. After initiation of treatment or cardiac tamponade recurs after pericardiocentesis with an unidentified etiological diagnosis, some authors recommend pericardioscopy, pericardial biopsy with histological and bacteriological examination.

[38], [39], [40], [41], [42], [43], [44]

Indications for consultation of other specialists

In acute idiopathic cases, the patient is administered by a cardiologist or therapist.

In complicated or specific cases of acute pericarditis (tuberculous, purulent, uremic, tumor), a multidisciplinary approach is required, including consultations of a cardiosurgeon and specialists (infectious disease specialist, phthisiatrist, nephrologist, endocrinologist, oncologist).

Treatment of acute pericarditis

With idiopathic and viral pericarditis treatment is aimed at reducing inflammation of the pericardium and relief of pain. In specific cases of acute pericarditis of known etiology, etiotropic treatment is possible; If pericarditis is a manifestation of a systemic disease, the treatment of this disease is performed.

Indications for hospitalization

Most patients with viral or idiopathic acute pericarditis (70-85%) can be treated on an outpatient basis, since the disease is usually benign, with symptoms persisting for about 2 weeks and a good response to NSAIDs. If there is a small or medium effusion, it dissolves within a few weeks. A second examination is not necessary if the symptoms do not resume or there is no deterioration.

To determine the indications for hospitalization, it is necessary to assess the presence of hemodynamic instability and the safety of outpatient treatment. The main indications for inpatient treatment are indicators of poor prognosis:

• fever above 38 ° C;
• subacute course of the disease;
• immunosuppression;
• connection of acute pericarditis with trauma;
• acute pericarditis in a patient taking oral anticoagulants;
• myopericarditis;
• large pericardial effusion;
• insufficient effect of NSAID treatment.

There are practical practical recommendations for short-term hospitalization of all patients with acute pericarditis to assess risk factors followed by 24-48 hours for an outpatient treatment of those patients who do not have risk factors and pain quickly passed with the initiation of NSAID administration. Emergency hospitalization and treatment in the intensive care unit is necessary for pericardial swelling with cardiac tamponade. Hospitalization is also mandatory if additional invasive studies are needed to establish the etiology of the disease.

Non-pharmacological treatment of acute pericarditis

Patients with acute pericarditis show a restriction of physical activity.

Drug treatment of acute pericarditis

The basis for the treatment of acute pericarditis - the use of NSAIDs - leads to the cessation of chest pain in 85-90% of patients with idiopathic or viral acute pericarditis for several days. According to the recommendation of the European Society of Cardiology (2004), it is preferable to use ibuprofen (fewer side effects and no adverse effect on coronary blood flow) at a dose of 300-800 mg every 6-8 hours for several days or weeks, until the pain or effusion disappears. Preferred NSAIDs are acetylsalicylic acid (aspirin), 2-4 g / day for the treatment of patients with pericarditis after myocardial infarction (since there is experimental evidence that other NSAIDs may worsen the formation of postinfarction cicatrix). Effective for alleviating pain in the early days of the disease can be parenteral administration of ketorolac (NSAIDs with pronounced analgesic effect) of 30 mg every 6 hours. Sometimes, with intensive pain, additional use of narcotic analgesics is necessary. There are also recommendations on the appointment in such cases of a short course of treatment with prednisolone inside at a dose of 60-80 mg / day for 2 days with a gradual complete withdrawal within a week. The effectiveness of adding statins to the NSAIDs (rosuvastatin 10 mg / day) for faster reduction of inflammation, noted in single studies, still needs to be confirmed and further evaluated. When using NSAIDs, protection of the mucous membranes of the gastrointestinal tract should be provided (as a rule, gastric secretion-inhibiting H +} K + -ATPase inhibitors are used). NSAIDs do not allow to prevent there the hell of the heart, the constriction of the pericardium or the relapse of effusion in the future.

The results of the recently published randomized study of COPE (Colchicine for Acute Pericarditis, 2005) allow a wider recommendation of the routine use of colchicine in the treatment of acute pericarditis. Patients with acute pericarditis with relapsing or continuing for 14 days of pain by the first day give 1-2 mg colchicine and then 0-5-1 mg / day in two divided doses (at least 3 months), alone or in combination with NSAIDs. This treatment is well tolerated, reduces the likelihood of cardiac tamponade and the outcome of constrictive pericarditis, most effective for the prevention of relapses of acute pericarditis.

Acute pericarditis usually responds well to treatment with glucocorticoids, but there is evidence that patients who took them at the onset of the disease are more likely to experience recurrence of acute pericarditis (presumably due to the experimentally confirmed probability of exacerbation of the virus infection). According to a randomized study of COPE, the use of glucocorticoids is an independent risk factor for recurrence of acute pericarditis, so their use can be considered only in the resistance of patients with poor general condition to NSAIDs and colchicine or in patients with autoimmune acute pericarditis. Prior to the appointment of glucocorticoids, a thorough examination is needed to clarify the etiology of acute pericarditis. Apply prednisolone orally at a dose of 1-1.5 mg / kg per day for at least a month, followed by a slow decrease in dose before cancellation. To cancel glucocorticoids follows within 3 months, then appoint colchicine or ibuprofen. There is evidence that in the case of autoreactive acute pericarditis, intrapericardial administration of glucocorticoids is not effective in increasing the risk of recurrence, but this limits the invasive nature of the method.

Features of treatment of acute pericarditis in the presence of pericardial effusion without the threat of tamponade:

• specific treatment of pericardial effusion depends on etiology;
• with idiopathic or viral acute pericarditis, as a rule, an effective anti-inflammatory treatment;
• shows the limitation of physical activity;
• it is necessary to avoid dehydration (erroneous administration of diuretics can lead to the development of cardiac tamponade with "low venous pressure");
• should avoid the use of beta-adrenoblockers that suppress the compensatory activation of the sympathetic system, and other drugs that reduce the heart rate;
• if the patient previously received anticoagulants, it is advisable to temporarily cancel them or replace the indirect anticoagulants with heparins,

Tactics of treatment with pericardial swelling with cardiac tamponade

• emergency pericardiocentesis or pericardial drainage (removing even a small amount of fluid leads to a significant relief of symptoms and improvement of hemodynamics;
• the removal of the entire effusion normalizes the pressure in the pericardial cavity, diastolic pressure in the atria, ventricles, blood pressure and cardiac output if the patient does not have concomitant constriction of the pericardium or other heart diseases). Pericardiocentesis is contraindicated in cardiac tamponade due to aortic dissection;
• replenishment of intravascular volume in preparation for drainage of the pericardium (small amounts of salt or colloidal solutions - 300-500 ml - may contribute to hemodynamics, especially with hypovolemia, dobutamine vasopressin in a dose of 5-20 mcg / kg per minute, dopamine less effective);
• absence of ventilation at positive pressure - this reduces venous return and cardiac output and can cause a sudden drop in blood pressure;
• monitoring of hemodynamics.

Echocardiographic signs of diastolic collapse of the right chambers of the heart in the absence of clinical signs of tamponade are not a mandatory basis for emergency pericardiocentesis. Such patients require careful clinical observation, since even a slight further increase in effusion can cause a cardiac tamponade. In some patients, echocardiographic signs of compression of the right divisions can pass for several days, and peri-cardiocentesis can be avoided.

Surgical treatment of acute pericarditis

Pericardiocentesis is indicated in the following cases.

• cardiac tamponade;
• suspected purulent or neoplastic pericarditis;
• very large sweating clinical manifestations, resistant to drug treatment during the week.

Draining pericardium through a permanent catheter (for several days) reduces the risk of repeated tamponade when fluid accumulation continues. Surgical drainage of the pericardial cavity is preferred in the case of purulent pericarditis, recurrent effusions, or the need for pericardial biopsy. In a small number of patients with acute pericarditis with frequent and severe relapses, in spite of drug treatment, surgical pericardectomy may be necessary.

Approximate terms of incapacity for work

In uncomplicated idiopathic acute pericardial period of incapacity for work is about 2-4 weeks.

[45], [46], [47], [48]

Further management

After acute acute pericarditis, patients need to be monitored by a cardiologist with a view to timely diagnosing the recurrence or attachment of constrictive pericarditis.

Treatment and prevention of relapses of acute pericarditis

Drug treatment - the results of a randomized CORE trial (Colchicine in Recurrent Pericarditis, 2007) indicate the effectiveness of treatment with colchicine for up to 6 months in combination with aspirin; traditionally used and other NSAIDs or prednisolone inside; In case of ineffectiveness of such treatment, with frequent relapses, immunopathological forms, the use of cyclophosphamide or azathioprine (in a dose of 50-100 mg / day) or peri-cardial administration of triamcinolone (300 mg / m ³ ) can be effective .

Pericardectomy or pericardial window are shown only with frequent and clinically expressed relapses, resistant to drug treatment. Before pericardectomy, patients should not receive glucocorticoids for several weeks.

Information for patients

Patients should be informed of the clinical symptoms of worsening of acute pericarditis and the threat of tamponade (increased dyspnea, reduced exercise tolerance), which should promptly seek medical attention in connection with the likely need for emergency treatment. Patients who had previously suffered acute pericarditis should be informed of the possibility of recurrence of the disease and symptoms (chest pain, dyspnea, palpitation), which require the appearance of a doctor and a re-examination.

How to prevent acute pericarditis?

Prevention of acute pericarditis is not carried out.

Prognosis for acute pericarditis

The outcome of acute pericarditis can be resorption of effusion when the inflammation subsides, less often - the organization of effusion with the formation of pericardial adhesions, partial or complete obliteration of the pericardial cavity. A small number of patients who have undergone this disease, in the future can develop constrictive pericarditis. Lethality depends on the cause. Idiopathic and viral pericarditis have a self-limited favorable course without complications in almost 90% of patients. Purulent, tubercular and tumor pericarditis have a more severe course: with tubercular pericarditis, death is reported in 17-40% of cases, with non-treated purulent pericardial lethality reaches 100%.