0% found this document useful (0 votes)
65 views13 pages

Understanding Pericarditis Basics

Pericarditis

Uploaded by

Ch Zee
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
65 views13 pages

Understanding Pericarditis Basics

Pericarditis

Uploaded by

Ch Zee
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 13

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.

You might also like