Topic pericarditis

1. PERICARDITIS
GUIDED BY:
DR.DILIP SIR
PREPARED BY:
UTKARSH
KUNJ
VIRALSINH

2. WHAT IS PERICARDITIS ?
PERI CARDI ITIS
Around the Heart Inflammation
DEFINITION : Pericarditis is defined as the
inflammation of the pericardium with or without
associated pericardial effusion.

3. STRUCTURE OF PERICARDIUM

4. WHAT IS PERICARDIUM ?
 Pericardium is a sac like covering which covers the heart
It composed of two layers :
 Fibrous pericardium: it is fibrous sheath which
maintains the position of the heart in the chest
 Serous pericardium : it is deep serous layer that forms
a double layer around the heart. It is divided into :
Inner visceral layer called epicardium
Outer parietal layer which is fused with fibrous part
pericardium.
Between these two layer of serous pericardium a thin
lubricating fluid is present which is of 50ml in amount.
The fluid allows the heart to slip around when it beats
during contraction and return to its normal position

5. PERICARDITIS
 Inflammation of the pericardium is defined as the
pericarditis with or without association of
pericardial effusions.
 It is divided into following types:
1. Acute (dry or effusive) pericarditis
2. Recurrent pericarditis
3. Chronic (effusive, adhesive, or constrictive)—
lasting three months or more.

6. IMAGE OF PERICARDITIS

7. AETIOLOGY OF PERICARDITIS
 Idiopathic or non-specific pericarditis
 Infectious : Bacterial, tuberculous, viral (coxsackie,
influenza, HIV, etc.),
 Auto immune disorders : Rhuematoid arthritis,
Dreesler’s syndrome, Scleroderma.
 Diseases in adjacent structures :Myocardial infarction,
aortic dissection, pneumonia, pulmonary embolism,
empyema
 Metabolic disorders : Uraemia, dialysis-related,
myxoedema
 Neoplastic disorders : Primary: Mesothelioma,
sarcoma, fibroma, lipoma and others Secondary
(metastatic or direct spread): Lung carcinoma,
lymphoma, carcinoid and others
 Trauma

8. ACUTE PERICARDITIS

9. ACUTE PERICARDITIS
 Acute pericarditis may be either dry or effusive.
 Effusive pericarditis involves presence of fluid in
excess of 50 mL in the pericardial cavity.
 Effusive pericarditis occcur when inflammation
leads to oedema which results in effusive acute
pericarditis

10. PATHOPHYSIOLOGY OF PERICARDITIS
Inflammation in pericardium
Release of metabolic toxin
High blood urea
Irritates serous pericardium which secrete
a thick fluid with fibrin strands &WBCs
The wall of pericardium appears
like a butter-bread appearance

11. CLINICAL FEATURES

12. SYMPTOMS
 Sharp retrosternal chest pain
 Pain is aggravated during inspiration, any
movement, swallowing, change in position
 Pain is relieved by sitting
 Referred pain in scapular ridge due to irritation of
phrenic nerves
 Constitutional symptoms like fever, bodyache,
malaise, joint pain, and anorexia.

13. SIGNS
 Pericardial rub is heard on auscultation
 High pitched scratching or crunching sound is heard
which is superficial. (3,4,5 left intercostal spaces)
 It should not be mistaken as a murmur

14. INVESTIGATION
 Patients with acute pericarditis usually have
evidence of systemic inflammation which are as
follows
 Leucocytosis,
 ESR
 Increased C-reactive protein.
 Troponin levels may also be elevated in acute
pericarditis due to some involvement of the
myocardium by the inflammatory process.

15. DIAGNOSIS
 Acute pericarditis can be accurately diagnosed by the
following traid of sign and symptom.
Typical pericardial chest pain
Pericardial
friction rub
Typical
ECG
changes

16. ECG CHANGES
Early in the course of acute
pericarditis, the ECG
typically shows diffuse ST
elevation in association with
PR-segment depression.
The ST elevation is usually
present in all leads except
for aVR, but in post
myocardial infarction
pericarditis the changes may
be more localised.

17. ELECTROCARDIOGRAPHY

18. ECHOCARDIOGRAPHY
 Echocardiography usually demonstrates at least a
small pericardial effusion or it may be normal.

19. PROGNOSIS
 Prognosis depends on the aetiology of acute
pericarditis.
 Acute benign or idiopathic forms have an excellent
prognosis, while the uraemic pericarditis is usually a
harbinger of death.
 Pericarditis due to rheumatic fever also has a good
prognosis.

20. TREATMENT
 Treatment for pericarditis should be targeted
towards the specific aetiology but most cases are
idiopathic or viral, so an empirical therapy is
required.
 Empirical therapy in form of NSAIDs or aspirin is
the first-line approach and mainstay of treatment.
 Anti-tubercular and antibiotic treatment should be
instituted whenever required along with supportive
therapy in the form of salicylates and
corticosteroids to bring about early relief and to
prevent formation of adhesions.
 Symptomatic treatment for the relief of fever and
pain may be provided with analgesics.

21. RECURRENT PERICARDITIS

22. RECURRENT PERICARDITIS
 Recurrent pericarditis may occur in up to 30% of
patients after an initial episode of
acute pericarditis.
 Recurrent pericarditis often occurs due to systemic
illness like
Viral infection
Autoimmune diseases
Myocardial infacrtion
 Generally recurrent pericarditis is idiopathic

23. PATHOPHYSIOLOGY
 The pathophysiology of idiopathic recurrent acute
pericarditis as a trigger or an autoimmune and
autoinflammatory cause in susceptible patients.
1. The presence of antinuclear antibodies is more
common in patients.
2. The presence of anti heart and anti-intercalated
disk antibodies of patients with idiopathic
recurrent acute pericarditis is induced by
overexposure to self-antigens secondary to
myocardial or pericardial disease: pericardiotomy,
myocardial infarction

24. PATHOPHYSIOLOGY
3. The presence of proinflammatory cytokines
(interleukin [IL]-6, IL-8, and interferon-γ) in the
pericardial fluid, but not in the plasma, indicating a
local inflammation
4. The incidence of pericardial disease in connective
tissue disease and vasculitis.

25. CLINICAL FEATURES
 Recurrent pericarditis occur after 4-6 week interval
of acute pericarditis.
 Recurrent pericarditis is defined as a recurrence
of chest pain associated with at least one of the
following objective evidence of disease activity:
 Fever
 Pericardial rub
 ECG changes
 Worsening pericardial effusion
 Elevation of biomarkers of inflammation (elevation
in white blood cell count

26. DIAGNOSIS
 The diagnostic criteria of recurrent pericarditis are
as follows:
1) Documented initial episode of acute pericarditis;
2) The reemergence of pericarditis type pain; and
3) It is associated with at least one of the following
signs: pericardial friction, evocative electrical
modifications, new or increased pericardial
effusion, elevated CRP, evidence of pericardial
inflammation by cross-sectional imaging MRI

27. TREATMENT
 Aspirin
 indomethacin
 ibuprofen are the most studied therapeutic
methods

28. CHRONIC CONSTRICTIVE
PERICARDITIS

29. CHRONIC CONSTRICTIVE
PERICARDITIS
 Chronic constrictive pericarditis (CCP) is defined as
a dense and rigid thickening of one or both layers of
the pericardium with adhesions resulting in
compression of the heart with impairment in the
diastolic filling.

30. ETIOLOGY
 The most common causes include:
 Tuberculosis
 Idiopathic and viral pericarditis
 Chest irradiation
 Collagen vascular disease
Post-cardiotomy
 Malignancy

31. PATHOPHYSIOLOGY
Inflammation persists in pericardium
Fluid and immune cells start moving in pericardial tissues
Immune cells lead to fibrosis of pericardium
Calcification of pericardium
Inelastic sheath making the wall of pericardium stiff
Hardening of the wall leads to
CONSTRICTIVE PERICARDITIS

32. PATHOPHYSIOLOGY
 The pathophysiological hallmark of pericardial
constriction is equalisation of the end-diastolic
pressures in all four cardiac chambers.
 This occurs because the filling is determined by the
limited pericardial volume, not the compliance of the
chambers themselves.
 Initial ventricular filling occurs rapidly in early diastole
as blood moves from the atria to the ventricles without
much change in the total cardiac volume.
 This results in the characteristic dip and plateau of
ventricular diastolic pressures.The stiff pericardium
also isolates the cardiac chambers from respiratory
changes in intrathoracic pressures, resulting in
Kussmaul’s sign

33. CLINICAL FEATURES

34. SYMPTOMS
 Dyspnea
 Fatigue
 Distension of the abdomen is present due to acites
and swelling of the feet.

35. SIGNS
 A deep ‘y’ descent (Frederick’s sign) is seen.
 JVP is raised and increases/fails to decrease during deep
inspiration (Kussmaul’s sign)
 Haemodynamic changes occuring in chronic
constrictive pericarditis are:
 Paradoxical pulse :Present in ≈ 1/3
 Equal left/right filling pressures : Present
 Systemic venous wave Prominent ‘y’ descent (M orW
shape)
 Inspiratory change in systemic venous
pressure:Increase or no (normal) change (Kussmaul’s
sign)
 ‘Square root’ sign in ventricular Present pressure

36. Kussmaul’s sign

37. ON EXAMINATION
 Inspection of the precordium reveals a ‘quiet’ heart
and prominent veins may be observed all over the
chest. A systolic retraction at the apex may be
observed.
 On palpation, a diastolic ‘tap’ or ‘shock’ may be
palpated. It is due to the rapid filling of the right
ventricle. Retractile apex is present. Because
pericardium is adherent to the chest wall.
 The characteristic finding on auscultation is the
‘pericardial knock’. This is a sound due to rapid
filling of the ventricle in the early rapid filling phase.
 The heart sounds are normal and usually no murmur
is heard.

38. INVESTIAGTIONS

39. ELECTROCARDIOGRAPHY
 The ECG findings are not characteristic but include
low voltage of the QRS complexes, flattening or
inversion of theT-waves and occasionally atrial
fibrillation.

40. CHEST X-RAY
 The heart size is usually normal or slightly smaller.
The characteristic finding of constrictive
pericarditis, however, is the calcification of the
pericardium.
 This is best seen in the left lateral or oblique views
and is present in about two-thirds of the cases.
 In the lateral view, if the calcification is seen in the
entire pericardium (i.e. anteriorly, inferiorly and
posteriorly) the appearance is termed as ‘egg-shell
pericardial calcification’

41. X-RAY:CONSTRICTIVE PERICARDITIS

42. TRANSESOPHAGEAL ECHOCARDIOGRAPHY
 Transoesophageal echocardiography is more
sensitive and accurate in determining pericardial
thickness.
 Doppler echocardiography is important in the
evaluation of patients with suspected pericardial
constriction.
 Doppler echocardiography frequently demonstrates
restricted filling of both ventricles with a rapid
deceleration of the early diastolic mitral inflow
velocity (E wave) and small or absent a wave.

43. DOPPLER ECHOCARDIOGRAPHY

44. CT/MRI
 CT and MRI allow accurate measurement of pericardial
thickness and some assessment of diastolic filling
patterns.
 Ancillary diagnostic findings include conical narrowing
of the ventricles, atrial dilation, and enlargement of the
inferior vena cava, hepatomegaly, and ascites.
 The right atrial tracings show a ‘M’ or ‘W’ shaped
pattern corresponding to the right ventricular
pressures.
 It has been observed that the pulmonary wedge
pressure, pulmonary artery diastolic pressure, right
ventricular end-diastolic pressure, mean right atrial
pressure and superior vena cava pressures tend to be
equal or near-equal in constrictive pericarditis.

45. DIAGNOSIS
 The combination of pulsus paradoxus, neck vein
signs, ascites and pericardial ‘knock’
 It can be differentiated with tricuspid valvular
diseases, restrictive cardiomyopathies and cirrhosis
of the liver because they have their characteristic
murmurs, which increase in intensity on deep
inspiration

46. PROGNOSIS
 Without surgery the prognosis is poor. Long-
standing cases of constrictive pericarditis develop
hypoproteinaemia due to a protein-losing
enteropathy.

47. TREATMENT
 Medical management of constrictive pericarditis,
especially in less severe cases, is aimed at relief of
fluid overload with careful administration of
diuretics and is at best, palliative.
 In case of constrictive pericarditis Pericardectomy is
performed in which pericardium is removed.