Topic 4 Pericarditis
Definition:
Pericarditis is a polyetiological infectious or non-infectious inflammation of the
pericardium, manifested by fibrous changes and / or accumulation of fluid in its
cavity. Pericarditis is often benign, remaining unrecognized, being a manifestation
or complication of the underlying disease. It is possible, as if isolated, acute or
chronic for the inflammation of the leaves of the pericardium without an
established reason.
Classification
I According to the etiological principle, the following is distinguished:
• Idiopathic pericarditis.
• Infectious pericarditis:
- viral (Coxsackie A9, B1-4, ECHO-8, EpsteinBarr, mumps, chicken pox, rubella,
cytomegalovirus, HIV, parvovirus B19, etc.);
- bacterial (Streptococcus pneumoniae, Neisseria meningitides, Haemophilus,
Mycoplasma pneumoniae, Chlamydia, Rickettsia, Borrelia burgdorferi.
Mycobacterium tuberculosis, etc.);
- fungal (Candida, Histoplasma, etc.);
- parasitic (Entamoeba histolytica, Echinococcus, Toxoplasma, etc.);
- tuberculous.
• Non-infectious pericarditis:
- in systemic autoimmune diseases (SLE, rheumatoid arthritis, ankylosing
spondylitis, systemic sclerosis, dermatomyositis, nodular periarteritis, Wegener's
granulomatosis);
- In autoimmune processes of the 2nd type (rheumatic fever, postcardiotomy
syndrome);
- in case of metabolic disorders (renal failure, uremia, myxedema, Addison's
disease, diabetic ketoacidosis; cholesterol pericarditis);
- traumatic - direct damage (penetrating injury of the chest, perforation of the
esophagus, foreign bodies) and indirect damage (non-penetrating injury of the
chest, irritation of the mediastinum);
- neoplastic - primary tumors; secondary metastatic tumors; lung carcinoma;
carcinoma of other localization; leukemia and lymphoma; sarcoma; other tumors;
- radiation.
Ii. The clinical classification of pericarditis includes the following forms.
A. Acute pericarditis (duration less than 6 weeks):
1. Fibrinous (or dry)
2. Exudative (serous-fibrinous. Purulent, putrid, hemorrhagic)
• with tamponade
• without tamponade
B. Subacute pericarditis (from 6 weeks to 6 months from the onset of the disease):
C. Chronic pericarditis (longer than 6 months):
1. Exudative (sero-fibrinous. Purulent, putrid, hemorrhagic)
• with tamponade
• without tamponade
2. Adhesive (adhesive)
3. Constrictive (squeezing)
• "Armored Heart"
Pathogenesis
In most cases, acute pericarditis begins with limited catarrhal and then fibrinous
inflammation, most often localized in the mouth of large vessels. The
inflammatory exudate which is formed at the same time in a small amount,
containing a large amount of fibrinogen, is exposed to the return absorption. Liquid
effusion fractions are effectively “sucked off” through the lymphatic vessels, and
fibrin filaments are deposited on the visceral and parietal pericardial leaves,
somewhat restricting their movement relative to each other and giving them a
rough folded appearance. The limited fibrinous pericarditis which is not followed
by accumulation in the pericardial cavity of any appreciable quantities of exudate
received the name of a dry pericarditis.
Further, if there is a total involvement in the inflammatory process of the heart
shirt, the back absorption of the exudate is disturbed and it begins to accumulate in
large numbers in the pericardial cavity. In these cases, they speak of effusive, or
exudative pericarditis. The inflammatory exudate may be serous, serofibrinous,
purulent, or hemorrhagic. The inflammatory fluid is initially located in the lower
diaphragm and posterior basal cavity of the pericardium, and then spreads to the
entire cavity.
Later (the subacute stage), as the inflammatory process subsides, the exudate is
absorbed, and granulation tissue grows in the pericardial sheets, which is then
replaced by connective tissue fibers. If this productive process is accompanied by
the formation of pronounced connective tissue adhesions between the sheets of the
pericardium, they speak of the so-called adhesive (adhesive) pericarditis.
Sometimes scar tissue obliterates the entire cavity of the pericardium, tightens the
visceral and parietal sheets, which ultimately leads to a pronounced compression of
the heart. Such an outcome of pericardial effusion was called constrictive, or
compressive pericarditis.
Clinical picture and diagnosis
Dry pericarditis
Dry (fibrinous) pericarditis is characterized by the limited nature of pericardial leaf
inflammation and the absence of inflammatory effusion in the pericardial cavity. In
most cases, dry pericarditis ends with recovery (only a slight thickening of the
leaves of the pericardium persists), less often it is transformed into a pericardial
effusion.
Complaints:
Non-specific manifestations of inflammatory syndrome: a slight increase in body
temperature, chilling, malaise, pain and heaviness in skeletal muscles.
Pain in the heart
1. Pain in the heart area is the main subjective manifestation of dry pericarditis.
2. The most characteristic features of pericardial pain are:
• constant, long and monotonous nature of pain;
• connection with the position of the body (pain aggravates in the supine position
and weakens in an upright position);
• communication with breathing and coughing (strengthening with a deep breath
and cough)
• lack of the cupping effect of nitroglycerin.
Sometimes patients complain of dry cough, shortness of breath, palpitations,
dysphagia, which are mainly reflex in nature.
Inspection: the forced sitting position of the patient in bed, which somewhat
reduces the contact with each other of the inflamed leaves of the pericardium, the
pain in the region of the heart becomes less intense. Shallow breathing.
Palpation: over the region of cardiac dullness, you can feel a weak low-frequency
tremor - a kind of equivalent of pericardial friction noise.
Auscultation: Pericardial friction noise with dry pericarditis is distinguished by the
following features: 1. Noise is heard exclusively in the area of absolute heart
dullness and is not performed anywhere. 2. Noise is not constant and can change
during the day in the same patient. 3. Pericardial friction noise increases: in the
patient's vertical and forward-inclined position; at maximum exhalation; when
pressed with a stethoscope on the chest wall.
Laboratory and instrumental studies
Laboratory data: non-specific. Possible leukocytosis, shift the blood to the left,
increased ESR, increased seromukoid, C-reactive protein,
hypergammaglobulinemia, etc.
Electrocardiogram:
• concordant (unidirectional) elevation of the RS – T segment in many ECG leads;
• absence of abnormal Q wave;
• inversion of a tooth of T in many assignments;
• a significant decrease in the ECG voltage (with the appearance of exudate in the
pericardial cavity).
Echocardiogram: In most cases, with limited dry (fibrinous) pericarditis on
EchoCG, no specific signs of the disease can be detected. If there is a more
common and pronounced pericardial inflammation, M-modal and two-dimensional
echocardiography reveals a thickening of the pericardial sheets, sometimes a small
discrepancy between the sheets (separation) and the appearance of a narrow echo-
negative space between them, indicating the presence of a very small amount of
exudate in the pericardial cavity.
Pericardial effusion
Exudative (effusion) pericarditis is characterized by widespread (total)
inflammation of the leaves of the pericardium, and therefore the absorption of the
resulting exudate is disturbed, and a large amount of inflammatory fluid
accumulates in the pericardial cavity.
Complaints:
Patients with infectious pericardial effusion complain of fever, chills, symptoms of
intoxication.
At the very beginning of the disease (stage of dry pericarditis), pains in the region
of the heart can be noted (see above), however, as the exudate accumulates and the
pericardial sheets diverge, the pain decreases and disappears. Nevertheless, many
patients still note a persistent feeling of heaviness in the region of the heart.
In more rare cases, symptoms associated with compression of nearby organs may
occur:
• trachea (barking cough);
• esophagus (a violation of the ingestion of food - dysphagia);
• lungs (shortness of breath);
• recurrent laryngeal nerve (hoarseness), etc.
Examination: with large volumes of pericardial effusion, patients often take a
forced sitting position in bed. In exudative pericarditis, this is due to the fact that in
the supine position, hemodynamic disturbances associated with impaired blood
flow to the heart are significantly aggravated. In particular, in the horizontal
position of the patient there is a sharp compression of the mouth of the superior
vena cava with exudate. As a result, the inflow of blood to the heart is disturbed,
cardiac output decreases, blood pressure decreases, tachycardia and shortness of
breath appear.
Sometimes you may notice some bulging of the anterior chest wall in the
precordial region, as well as slight swelling of the skin and subcutaneous tissue in
the heart region (perifocal inflammatory reaction).
The configuration of the heart acquires a peculiar triangular or trapezoidal shape.
Palpation: the apical impulse is weak or not palpable at all.
Percussion: the borders of the heart are extended in all directions, an absolutely
blunt percussion sound is defined almost over the entire surface of the heart.
Auscultation: in the initial stages of the disease (stage of dry pericarditis) over the
area of absolute dullness of the heart, a pericardial friction noise can be heard (see
above). However, as the exudate accumulates in the pericardial cavity, the
pericardial friction noise disappears due to the lack of contact between the
pericardial sheets.
As a result of the posterior displacement of the heart, the heart tones become
audible medial to the apical impulse, and in the lower left regions of cardiac
dullness they are sharply weakened.
Laboratory and instrumental studies
X-ray examination: note an increase in the shadow of the heart, smoothing of the
heart contour, the disappearance of the "waist" of the heart. The shadow of the
vascular bundle becomes short.
Echocardiogram: detect the separation of the pericardial sheets with the formation
of echo-negative space behind the posterior wall of the LV.
The clinical picture of pericardial effusion, complicated by cardiac tamponade.
The clinical picture is usually dominated by symptoms associated with a decrease
in venous blood flow to the heart and low cardiac output:
• progressive general weakness and inability of patients to perform even minimal
exercise;
• heartbeat (tachycardia of reflex origin);
• dizziness, and in severe cases, transient disorders of consciousness, indicating
insufficient brain perfusion;
• increasing shortness of breath.
The compression of organs, vessels, and nerve trunks located in close proximity to
the heart (trachea, esophagus, vena cava, recurrent laryngeal nerve, etc.) often
leads to the following symptoms:
• cough (tracheal compression);
• dysphagia (esophagus suppression);
• hoarseness (compression of the recurrent laryngeal nerve) and others.
Finally, with a slow progression of the cardiac tamponade and its prolonged
existence, signs of venous congestion in the systemic circulation are increasing,
and an enlarged liver and the appearance of ascites usually precede the appearance
of peripheral edema. In this case, patients present the following complaints:
• pain in the right hypochondrium associated with an increase in the size of the
liver;
• increase in abdominal volume (ascites);
• dyspeptic symptoms, weight loss and anorexia caused by venous congestion in
the portal system and dysfunction of the abdominal organs.
• the appearance of edema of the lower extremities
Examination and examination of the abdominal organs and lungs
Patients usually occupy a forced position. They sit in bed, the torso is tilted
forward, and seems to be frozen in a pose of a deep bow. Sometimes patients
kneel, resting their forehead and shoulders on a pillow (Breitman posture).
Characterized by pallor of the skin, often in combination with diffuse gray
cyanosis, cooling of the limbs. In the event of attacks of severe weakness,
accompanied by a fall in blood pressure, frequent thready pulse, pallor and
cyanosis increase, sticky cold sweat and other symptoms characteristic of
cardiogenic shock appear.
In the study of the lungs, the absence of moist rales and other signs of blood
stagnation in the small circulation system is noteworthy, despite the presence of
increasing shortness of breath in patients with heart tamponade.
Examination of the heart: During examination, palpation, percussion and
auscultation of the heart in patients with tamponade usually show the same
changes as in exudative pericarditis without compression of the heart chambers:
A distinctive feature of exudative pericarditis, complicated by cardiac tamponade,
is the paradoxical pulse (decrease in systolic blood pressure on inspiration by more
than 10–12 mm Hg).
Laboratory and instrumental studies
Electrocardiogram:
• low ECG voltage;
• relatively short-term elevation of the RS – T segment in several leads;
• nonspecific changes of the T wave (smoothness, inversion).
Echocardiography:
1. Reduction of collapse on inspiratory inferior vena cava.
2. Dimensions of the pancreas and LV cavity are usually reduced.
3. During expiration, diastolic collapse of the pancreas can be observed.
4. When Doppler study can detect a significant increase in pressure in the pancreas,
PP, as well as the filling pressure of the pancreas,
5. Finally, in patients with cardiac tamponade, as well as in all patients with
pericardial effusion, pericardial leaflets and the presence of fluid in the cavity are
detected.
X-ray examination: with a significant effusion in the pericardial cavity, the size of
the heart shadow is increased, and the contours are smoothed. The shadow of the
heart is in the middle.
Constrictive pericarditis: (from the Latin. Constrictio - compression) is
characterized by thickening of the leaves of the pericardium, obliteration of its
cavity, often by calcification of the pericardium, which leads to compression of the
heart and violation of the diastolic filling of the heart chambers.
Constrictive pericarditis is characterized by the following hemodynamic features:
1. Violation of diastolic filling of both ventricles, accompanied by increased KDD
in the ventricles and medium pressure in the atria, as well as preservation of
normal contractility of the ventricles.
2. Increased venous pressure and blood stagnation in the major circulation, mainly
in the portal vein system (suprahepatic portal hypertension).
3. The absence of venous stasis of blood in the lungs.
4. A decrease in stroke volume and a tendency to a decrease in blood pressure and
perfusion of peripheral organs and tissues. 5. Small or normal size of the ventricles
of the heart.
Complaints: in typical cases, the presence of the so-called “Beck triad” is
characteristic:
• high venous pressure;
• ascites;
• “small quiet heart”.
Examination and examination of the abdominal organs and lungs
With a significant compression of the mouth of the superior vena cava, the face
becomes puffy, the neck looks thickened, edematous, the skin of the face and neck
acquires a pronounced cyanotic coloration, and the neck veins are swollen. Edema
and cyanosis spread to the head and shoulders. Such a symptom complex, called
the Stokes Collar, indicates a significant impairment of blood flow through the
superior vena cava.
It should be emphasized that ascites and severe hepatomegaly usually precede the
appearance of edema in the legs, which is also a very characteristic sign of
constrictive pericarditis. Often, it is these two symptoms (ascites and
hepatomegaly) that prevail in the clinical picture of the disease, resembling the
clinical manifestations of cirrhosis of the liver (“pseudocirrosis” of Peak).
Examination of the heart and blood vessels: important signs of constrictive
pericarditis are dilation and swelling of the neck veins, which persist even after
intensive diuretic therapy. At the same time, unlike the cases of cardiac tamponade,
the pulsation of the veins is clearly visible, in particular, their diastolic collapse
(Friedreich symptom),
Moreover, the venous pressure and, accordingly, the swelling of the cervical veins
increase markedly on inspiration (Kussmaul symptom).
On palpation of the heart, the apical impulse, as a rule, cannot be detected, and
epigastric pulsation is also absent. With a deep breath, an unusual systolic
depression or retraction of the lower part of the sternum and intercostal spaces can
sometimes be determined. This phenomenon indicates the presence of adhesions
between the outer sheet of the pericardium and the anterior wall of the chest and
diaphragm.
The boundaries of the heart in most cases are not extended. Interestingly, when
changing the position of the body (for example, when the patient turns to the left
side), the borders of the heart do not move, since the fixed cicatrical shell, which
encloses the heart, is fixed to the mediastinum.
When auscultation I and II tones are deaf. Often determined by the three-term
rhythm (canter rhythm).
Laboratory and instrumental studies
Electrocardiogram:
• low voltage of the QRS complex;
• negative and biphasic T teeth in all standard and chest leads;
• advanced high P wave or atrial fibrillation.
X-ray examination:
• a relatively small or normal heart (more precisely, the ventricles), while
simultaneously increasing the size of the atria;
• lack of a “waist” of the heart and differentiation of arcs due to the characteristic
straightening of the heart contours;
• irregularity of the contours of the heart due to the presence of numerous
pericardial adhesions;
• pericardial calcification, found in about 1/3 of patients with constrictive
pericarditis.
Adhesive (adhesive) pericarditis is characterized by the presence of pronounced
connective tissue adhesions between the sheets of the pericardium, sometimes
formed during resorption of the exudate, proliferation of granulation tissue, which
is then replaced by connective tissue fibers.
“Crustacean heart” is a variant of compressive pericarditis, in which calcification
of the pericardium occurs, which turns into a rigid, dense, slow-moving bag
(armor) surrounding the heart.
Treatment of pericarditis:
The choice of the most appropriate treatment for acute pericarditis depends on the
clinical and morphological form of the disease and its etiology.
1. Acute (fibrinous or exudative) pericarditis
In most cases, limited to the appointment of non-steroidal anti-inflammatory drugs
(NSAIDs):
• diclofenac (voltaren) - 100–200 mg per day;
• indomethacin - 25–50 mg every 6–8 h; • Ibuprofen - 400–800 mg;
Glucocorticoids should be prescribed only in the following clinical situations:
• with intensive pain syndrome that is not amenable to treatment of NSAIDs;
• in severe cases of diffuse connective tissue diseases (systemic lupus
erythematosus, rheumatoid arthritis, polymyositis, etc.), complicated by acute
pericarditis;
• with allergic medicinal pericarditis;
• with autoimmune acute pericarditis.
Daily doses and duration of administration of glucocorticoids are selected
depending on the etiology and nature of pericarditis and the underlying disease. In
case of intense pain syndrome, for example, glucocorticoids are prescribed in a
daily dose of 40–60 mg for 5–7 days, followed by a lowering of the dose and
withdrawal of the drug.
For viral (idiopathic) pericarditis, it is recommended to refrain from using
glucocorticoids (M. Freed, J.D. Band).
Antibiotics for dry (fibrinous) pericarditis are prescribed only in cases when the
inflammation of the heart shirt arises against the background of a clear bacterial
infection - sepsis, infective endocarditis, pneumonia, presence of a purulent focus,
etc.
2. In case of purulent exudative pericarditis, in addition to parenteral
administration of antibiotics, pericardiocentesis is shown with the maximum
removal of exudate, washing the cavity and repeated introduction of antibiotics
into the pericardial cavity (through the catheter).
3. At tamponade of the heart, an emergency (for health reasons) pericardiocentesis
with exudate removal is indicated.
4. With constrictive pericarditis - subtotal pericardiectomy
Forecast:
In most cases, the prognosis of dry (fibrinous) pericarditis is quite favorable.
Finally, in approximately 1/4 of the cases, transformation of dry (fibrinous)
pericarditis into exudative (exudative) and even (rarely) into constrictive
(squeezing) pericarditis is possible.
With acute pericardial effusion in most cases, recovery occurs in 2-6 weeks.
Cardiac tamponade develops in approximately 15% of patients with acute
pericarditis, and the outcome in constrictive pericarditis is observed in 10% of
patients.
The long-term prognosis of constrictive pericarditis depends on the effectiveness
of the surgical intervention (pericardectomy). In most cases, a successful operation
provides a high survival rate. In the absence of surgical treatment, the prognosis is
poor.