Pericarditis

Dononbaeva N.
A
Pericarditis is an infectious or non-
infectious (aseptic) inflammation of the
visceral and parietal pericardium.
Etiology
Infectious
Viral infection (Coxsackie viruses, ECHO, influenza, herpes, adenovirus, etc.)
Bacterial infection (pneumococci, staphylococci, meningococci, streptococci,
mycobacterium tuberculosis, chlamydia, salmonella, etc.)
Fungal infection
Rickettsia
Ionizing radiation, X-ray therapy
Malignant tumors (metastatic lesions, primary pericardial
tumors)
Hemoblastosis
Hemorrhagic diathesis
Non-infectious
Allergic diseases (serum sickness, drug allergy, etc.)
Diffuse connective tissue diseases (SLE, rheumatoid arthritis, systemic scleroderma,
rheumatism and etc.)
Myocardial infarction (episthenocarditis pericarditis and pericarditis in postinfarction
Dressler syndrome)
Diseases with severe metabolic disorders (hypothyroidism, uremia, gout,

)
amyloidosis, etc.
Chest trauma
Ionizing radiation, X-ray therapy
Malignant tumors (metastatic lesions, primary pericardial tumors)
Hemoblastosis
Hemorrhagic diathesis
Clinical and morphological classification
of pericarditis
Acute pericarditis (less than 6 weeks from onset):
1. Catarrhal
2. Dry, or fibrinous.
3. Effusion, or exudative (serous, serous-fibrinous, purulent,
hemorrhagic):
 without cardiac tamponade;
 with cardiac tamponade.
Subacute pericarditis (6 weeks to 6 months from onset):
1. Exudative.
2. Adhesive.
3. Compressive, or constrictive:
Chronic pericarditis (more than 6 months from the onset
of the disease):
1. Exudative.
2. Adhesive.
3. Compressive, or constrictive.
4. Compressive with calcification ("armored heart"):
Dry or fibrinous pericarditis
Limited fibrinous pericarditis, not accompanied by the
accumulation in the pericardial cavity of any noticeable
the amount of exudate,
This is the most common form of acute pericarditis.
In most cases, acute pericarditis begins with a limited catarrhal,
and then fibrinous inflammation, most often localized in the mouth
of large vessels. Formed with a small amount of inflammatory
effusion containing a large amount
fibrinogen, is reabsorbed. Liquid fractions of effusion effectively
are “sucked off” through the lymphatic vessels, and fibrin
filaments are deposited on the visceral and parietal sheets of the
pericardium,
Clinical sings
 Pain in the chest - dull, monotonous, not too intense pain that is localized
behind the sternum or to the left of it and radiates to both arms, trapezius
muscles, the epigastric region. pain can last for hours and days. A
characteristic feature of pericardial pain is its intensification in the patient's
position. lying on your back, with a deep breath, coughing and swallowing.
Pain is often relieved by sitting and with shallow breathing. Nitroglycerin
does not relieve pain.
 nonspecific manifestations of the inflammatory syndrome: small increased body
temperature, chills, malaise, pain and heaviness in skeletal muscles.
examination
orthopnea ( slightly reduces contact with each other inflamed pericardium)
Superficial , rapid breathing.
palpation and percussion of the heart no specific
signs
Auscultation
pericardial rubb superficial stretching sound produced by
movement of inflamed pericardium, localized to a small area
over the pericardium, best heard to the left of the lower
sternum, usually in systole but my be audible in diastole.
Friction is best heard when the patient learns forward,
diaphragm of stethoscope is pressed firmly upon the chest,
the patients breath being held for a time in inspiration and
than in expiration.
Arterial pulse and blood pressure with dry pericarditis
practically do not change
Laboratory data are non-specific. leukocytosis, shift of
the blood count to the left, an increase in ESR, an increase
in the content of seromucoid, C-reactive protein,
hypergammaglobulinemia
Electrocardiogram in acute pericarditis, elevation of the
RS-T segment is recorded in most standard, limb and in
several chest leads. ( with acute pericarditis, as a rule, there is a large lesion
area, affecting many areas of the heart muscle). C oncordant (unidirectional)
elevation of the RS-T segment,
treatment
depends on the clinical and morphological form of the disease
and its etiology.
Newly diagnosed acute pericarditis requires hospitalization of
the patient and restrictions physical activity.
regularly monitor the levels of arterial and venous pressure and
heart rate.
Repeated echocardiographic studies (timely diagnosis of the formation of
effusion in the pericardial cavity )
NSAIDs: diclofenac (voltaren) - 100-200 mg per day;

indomethacin - 25-50 mg every 6-8 hours;
ibuprofen - 400-800 mg;
glucocorticoids only in the following clinical situations:
with intense pain syndrome that does not respond to NSAID treatment; In severe cases of diffuse
connective tissue diseases; with allergic drug pericarditis; with autoimmune acute pericarditis.
prognosis
In most cases, predicting dry (fibrinous) pericarditis
is quite favorable. Against the background of
adequately prescribed therapy, there is a rapid
decrease in signs of inflammation.
Thank you for attention!
Exudative (effusion) pericarditis
characterized by widespread (total) inflammation of the
pericardial leaves, in connection with which the absorption of the
resulting exudate is impaired, and a large amount of
inflammatory fluid accumulates in the pericardial cavity.
Slow accumulation of inflammatory exudate, accompanied by a
gradual stretching of the external pericardial leaf, filling of
pericardial pockets and a slow increase in the volume of the
cavity. In these cases, the increase in intrapericardial pressure is
not long occurs and intracardiac hemodynamics does not change
markedly.
Cardiac temponade- if pericardial effusion accumulates very
quickly, stretching of the outer layer of the pericardium, adequate
to the increased volume of inflammatory fluid, does not occur,
and the pressure in the pericardial cavity increases significantly.
This leads to compression of the heart chambers and a sharp
decrease in diastolic ventricular filling.
with external compression of the heart, first of all, the diastolic
filling of the right ventricle is disturbed, blood stagnation occurs in
the veins of the systemic circulation, while a relatively small
volume of blood enters the pulmonary artery. As a result, the
preload is reduced by LV, its shock ejection and perfusion of
peripheral organs and tissues is impaired, while LV filling pressure
remains normal or low.
pericardial
pressure
Complaints: a feeling of heaviness in the region of the heart.
Symptoms of specific etiology may be present. In more rare
cases, symptoms associated with compression of nearby
organs may appear.
Examination: orthopnea (obstruction of blood flow to the heart), some
bulging of the anterior chest wall in the precordial region, slight
swelling of the skin and subcutaneous tissue in the region of the
heart (perifocal inflammatory reaction).
palpation: Apical impulse is weakened or not palpable at all.
percussion: The boundaries of the heart are expanded in all
directions. The configuration of the heart becomes triangular or
trapezoidal forms. The boundaries of cardiac dullness vary
depending on the position of the patient's body.
Configuration of the heart

with exudative pericarditis
Auscultation: as you ac accumulate in the pericardial
cavity of the exudate, the pericardial friction noise
disappears due to the lack of contact between pericardial
sheets.
Arterial pulse and blood pressure: In the absence of
signs of compression (temponade) of the heart, blood
pressure may not be changed. In cardiac temponede falling
blood pressure, paradoxical pulse.
a - during inspiration, there is an increase in blood flow to the right heart, a
displacement of the IVS towards the left ventricle and limiting its volume; b -
during exhalation - collapse of the RV and the RV and displacement of the IVS
towards the RV
Chest x-ray: an increase in the shadow of the heart,
smoothing of the cardiac contour, the disappearance of the
"waist" of the heart. The shadow of the vascular bundle
becomes short. The phenomenon of visual shortening of the
aorta.
Echocardiography: demonstrates pericardial effusion. Diastolic
collapse of right atrium and right ventricle is the most useful
echo signs of temponade.
Сardiac catheterization in temponade: low cardiac output,
elevated equal or near equal pressures in all four chambers.
ECG in temponade: changes in the amplitude of the QRS
complex due to the displacement of the heart, as if “floating”
inside the inflammatory fluid.
Puncture of the pericardial cavity: carried out for diagnostic
and therapeutic purposes. Main indications for puncture are:
 growing symptoms of cardiac tamponade (usually a puncture is performed
urgently, in order to evacuate fluid and reduce compression of the heart);
 suspicion of purulent exudative pericarditis;
 no tendency to resorption of exudate (prolonged course of effusion
pericarditis);
 clarification of the nature of effusion pericarditis.
treatment
 The tactics of treating acute pericardial effusion
without cardiac compression is basically the same as and
dry pericarditis.
 Strict and regular control (includ. echocardiog) of the
main hemodynamic parameters.
Antibiotics for bacterial exudative pericarditis, or
purulent pericarditis.
 with cardiac tamponade for emergency
pericardiocentesis. Preliminary for hemodynamic stabilization
intravenously injecting 300-500 ml of plasma, colloidal solutions or 0.9%
solution sodium chloride, as well
as inotropic agents (digoxin, dobutamine).
prognosis
In acute exudative pericarditis, in most cases, recovery
occurs after 2–6 weeks. Cardiac tamponade develops in
about 15% of patients with acute pericarditis, and the
outcome in constrictive pericarditis is observed in 10%
of patients. Often, the prognosis is determined by the
nature, severity and the adequacy of therapy for the
underlying disease, complicated by pericarditis.
Thank you for attention!

Pericarditis

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Pericarditis

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Dononbaeva N.

Diseases with severe metabolic disorders (hypothyroidism, uremia, gout,

NSAIDs: diclofenac (voltaren) - 100-200 mg per day;

Configuration of the heart

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