PERICARDITIS

PERICARDITIS

• BY— PRIYANKA BHOWMIK

• GROUP—5

• SEMESTER —8
• It is fibroelastic PERICARDIUM
sac.
• Contains 15 to
50ml of ultra-
filtrate of plasma.
Clinical classification Duration

Acute pericarditis < 6 weeks

Subacute pericarditis 6 week to 6 months

Chronic pericarditis >6 months

 Classification by etiology

1) infective pericarditis

2) hypersensitive reaction/ autoimmune process

3)non infective, non-immune/ miscellaneous causes of pericarditis

• 90% to 85% cause is idiopathic/viral.

Causes of Infective pericarditis

COxsackei B, coxsackei A,EBV, mumps virus,

Virus
hepatitis B&C virus, HIV, adenovirus

Staphylococcus aureus, streptococcus, pneumococcus,

Pyogenic
nisseria, leigionella, burilia burgdogpheri,
bacteria
mycobacterium

Histoplasma capsulatum, coccidioidomycosis,

Fungal
blastomycosis, Candida albicans, aspergillosis

Parasites Toxoplasma, echinococcus

 HYPERSENSITIVITY/
AUTOIMMUNE CAUSES
• Rheumatic fever

• SLE

• Rheumatoid arthritis

• Sclerodermatitis

• Drug induced- Hydralyzine,isoniazid, penicillins,

procainamide,phenytoin.

• Post-trauma — after several weeks

• Post cardiotomy —after ~ 4 weeks

 MISCELLANEOUS CAUSES
• Acute myocardial infarction

• Uraemia - most common cause in developed

countries. Do dialysis till pericardial rub disappears.

• Neoplasia

• Myxedema

• Trauma

• Radiation
Types of acute and subacute pericarditis
 Serous Heamorr-
Types Fibron-ous Supra-tive Caseous
pericard-itis hagic

Moderate to
Severity Mild Moderate Severe Severe
Severe

Mycoplasma
Infective Infective+ Pyogenic
Causes Malignancies tuberculosis,
causes autoimmune bacteria
Fungal

Albumin+ Albumin+ Thin Fluid+

Exudate
globulin+ globulin+ yellowish Blood +fluid fibrin+
contains
wbc fibrin+wbc creamy pus calcium

Good Good Poor Poor

Healing Organization
prognosis prognosis prognosis prognosis
Types of chronic/healed pericarditis
1) soldier’s plaques

• Some areas of pericardium is thickened without

loss of function

• Milk spots

• Multiple fibrotic plaques

2) adhesive pericarditis

• Very thin and fine fibrous bands are present

• Not dangerous because not enough to retract and

cause heart problems

• No loss of function
3)adhesive mediastinopericaditis
• Fibrin strings attaches to
heart and also to
neighbouring structures like
lungs

• Pericardium is heavily
colonised by fibrin

• Strain on cardiac function

may lead to hypertrophy and
dialation
4)constructive pericarditis
• Heavily colonised fibrinogen

• Secondary to — caseous
pericarditis, suprative
pericarditis, hemorrhagic
pericarditis

• Form rigid fibro-calcific

mass which eventually
shrinks the heart

• Ventricular filling is
improper ,leading to diastolic
DIAGNOSIS
1)Chest pain

2)pericardial rub

3)ECG changes

4)Pericardial effusion
 CHEST PAIN
Pericarditis pain Ischemic heart disease pain
Sharp,well localised,stabbing pain Dull, diffuse, crushing, constricting
pain
Central chest pain, pericardial pain, Central chest pain, pericardial pain,
retrosternum pain retrosternum pain

Pleural pain present on coughing, deep No changes or no relation of pain with

inspiration coughing or deep inspiration

Relief or reduce in pain on bending Relief of pain on resting, or by

forward, increases on lying position. nitroglycerin intake.
It is postural pain. It is not postural pain.

Pain radiates or may not radiate. Mostly radiates to neck, hands,jaw

Scapular angle pain, in trapezoid ridge
is hallmark.
• Pleural pain
disappears on holding
the breathe whereas
pericarditis pain don’t.

• Note all pericarditis

patients don’t always
come with typical
sharp stabbing pain

• Gradually developing
pericarditis maybe
painless, examples -
tuberculosis
pericarditis, post
radiation, uremic
 PERICARDIAL RUB
• Present in 85% of patients

• Very loud scratchy sound on auscultation

• Best heard in left sternal point at end of expirations

• Rub can be monophasic, biphasic, triphasic

• Pleural rub disappears on holding breath whereas

pericardial rub don’t.
 ECG CHANGES
• Classical ecg of pericarditis has 4 Stages.

• Stage 1- ST segment elevation with PR segment depression

• Stage 2-ST segment and PR segment goes to normal position

• Stage 3- T wave inversion

• Stage 4- T wave returns to normal position

 Pericarditis STEMI
ST elevation is concave upwards, ST elevation is concave downwards.
saddle shaped.

Usually PR segment depression seen Very rarely seen PR segment

due to atrial inflammation depression as atrial infarction is rare.

Diffuse ST elevation, except aVR and ST elevation only on leads facing the
V infarcted area, opposite leads have
reciprocal changes.

T waves never show changes until ST T wave and ST segment changes may
segment is back to normal show up simultaneously

Biomarkers troponin T&I, CKMB Troponin T&I, CKMB level is very

mild elevation high.
 Pericardial effusion
• As effusion progress— pericardial rub disappears

• Loss of palpable apex beat

• If rapid fluid accumulation occurs it leads to cardiac

tamponade
• Lungs are
compressed badly

• Ewart’s sign-
bronchial sound is
present, Dull on
percussions,
increase vocal
fermitis/egophony.
 Investigation
• Echocardiography - best investigator method. It’s non-invasive,
simple, specific, good sensitivity and can be done on bedside.

• CT

• MRI

• Chest X-ray

• Lab test - checking bio markers, inflammatory markers, increase

ESR, CRP, TLC

• Urine, creatinine if suspect uremia

 Treatment
• Symptomatic relief - bedrest, monitoring for complications

• NSAIDs - contraindicationed in acute MI patients

• Colchicine

• Steroids

• Cyclophosphamide, methotrexate

• Pericardiocentesis/ pericardial drainage

• Pericardiectomy
 THANK YOU !!!

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