PERICARDIAL DISEASE

2. OUTLINE
 Brief anatomy and physiology
 Clinical classification
 Causes
 SxS of each variant of pericarditis
 Work-up of each variant of pericarditis
 Management of each variant of pericarditis

3. Anatomy & function
 Fibrous sac surrounding heart-dense
network of collagen fibres
 Serous membrane – two continuous layers
separated by a small amount of fluid
lubricant (10-20mls straw coloured)
 Layers are called visceral and parietal
 Surrounds the heart

4. …Anatomy & function
Continuous with the great arteries and
the diaphragm
 Stabilises the position of the heart within the chest
 Prevents friction between the moving heart and
adjacent structures
 Allows for small acute changes in size and shape but
limits ventricular filling

6. Pathophysiology
 Significantly increased intrapericardial pressure
impedes diastolic filling of the ventricles
 Therefore in order for the ventricles to fill the end-
diastolic pressure must exceed the pericardial
pressure
 Global effusion – pericardial pressure is equal
around heart
 Therefore both ventricles have to increase EDP to
same amount for ventricles to fill

7.  Normal difference in diastolic pressures between RV
and LV is lost
 As the pericardial effusion worsens the EDP cannot
raise significantly to maintain cardiac output

8. ETIOLOGY OF PERICARDITIS
A. INFECTIOUS PERICARDITIS
1. Viral (coxsackieviruses A and B, echovirus,
mumps, adenovirus, Epstein-Barr, human
immunodeficiency virus, influenza)
2. Mycobacterium tuberculosis Bacterial
(Pneumococcus, Streptococcus,
Staphylococcus, Legionella)
3. Fungal (histoplasmosis, coccidioidomycosis,
candidiasis, blastomycosis) Other (syphilis,
parasites, Q fever

9. B. NONINFECTIOUS PERICARDITIS
1 . Idiopathic
2. Neoplasm Metastatic (lung cancer, breast cancer,
melanoma, lymphoma) Primary (mesothelioma)
3. Renal failure
4. Irradiation
5. Myocardial infarction
6. Hypothyroidism
7. Aortic dissection with hemopericardium Chylopericardium
(thoracic duct injury)
8. Trauma : Post pericardiotomy ,Chest wall injury or
trauma
9. . Pneumonia

10. C. HYPERSENSITIVITY PERICARDITIS
1. Collagen vascular disease (systemic lupus
erythematosus, rheumatoid arthritis,
scleroderma,
acute rheumatic fever, Sjögren's syndrome, Reiter's
syndrome, ankylosing spondylitis)
2. Drug induced (procainamide, hydralazine,
isoniazid; smallpox vaccine)
3. Post myocardial infarction (Dressler's syndrome)
4. Familial Mediterranean fever

11. Pericardial disease
 Acute- primary –Idiopathic
 Chronic
- Constrictive
- Effusive
- Constrictive-effusive

13. Causes
Idiopathic (idiopathic) – 86%
 Infective (viral or bacterial) – 7%
 Following a myocardial infarction or cardiac
surgery (Dressler’s syndrome)
 Radiation therapy
 Neoplastic disease (commonly lung or breast) –
6%
 Connective tissue disease

14. Patient approach
Results from an inflamed &
thickened pericardium w/c affects
the heart’s function.
 Clinical examination
 Auscultation
 Chest x-ray
 ECG
 Echo

15. General Symptoms pericarditis
1. Retrosternal chest pain – sharp worse on
insp and bending forward.
2. Friction rub (high pitched scratching
noise)
3. Raised jugular venous pressure
4. Other associated symptoms
Depending up on the cause.

16. Diagnosis of pericarditis
 Characteristic chest pain
 Pericardial friction rub (auscultation)
 ECG showing characteristic ST elevation
(caused by epicardial injury)

17. Differentiating from MI
 ST elevation –diffuse
 Shape
 Q waves
 ST –T changes with time
 History of the patient
 Cardiac enzymes etc

18. Treatment
 Search for the underlying disease and treat
 Patients require bed rest
 NSAID (aspirin, indomethacin) are effective for
relieving symptoms of chest pain
 Steroid in selected cases

19. Prognosis
 Pericarditis is usually a benign disorder but,
depends up on the cause
 Diagnosis relates to underlying cause
 But any cause can lead to an effusion and tamponade
which can lead to death
 Pericarditis can also progress to pericardial
constriction and heart failure

21. Causes
 Tuberculous pericarditis.
 Post-radiotherapy
 post-surgical causes.
 Needs to be differentiated from restrictive
cardiomyopathy when making diagnosis.

22. Signs Kussmauls sign
 Normal subjects – inspiration causes a decrease in
chest pressure. Increase in venous return – JVP falls
 In Constrictive pericarditis – Increased venous return
cannot be accommodated in VR because of high EDP
 So JVP rises on inspiration
Signs

23. Investigations
As for acute pericarditis;
 Clinical examination – prime symptoms likely to be RHF
and SOB
 ECG may not show characteristic ST elevation
 CXR may see calcification and helps to rule out coexisting
effusion
 Echo to identify haemodynamic effects on heart and
coexisting effusion
 Auscultation may reveal a friction rub
 MRI/CT scan – data about the thickness of the
pericardium. Cine CT is a new technique which also gives
info about the effects of physiology as well.

24. Chest x-ray
 Occasionally
calcification noted
 More useful to
determine whether
there is a coexisting
effusion (fluid
accumulation)

25. Echo findings
 Normal subjects – increase in TV flow velocity on
inspiration, and decrease in MV flow
 Due to increased vascular capacity of lungs
venous return and RV output increases while
return to LA is reduced
 This is exaggerated in tamponade/sig constriction
– RV output can’t increase because of high EDP +
pulmonary return is reduced further

26. Treatment
 The only effective treatment for chronic
constrictive pericarditis is complete surgical
resection of the pericardium.
 Mortality for procedure ranges from 5-16%
 Symptomatic improvement in ~90%
 5 year survival rate is 74-87% depending on co-
morbidities pre-op

27. Pericardial effusion
 Acute
 Chronic
 Global
 Localized

28. Pericardial effusion
 Spectrum of causes of effusion is similar to acute
pericarditis
 More likely than constriction following MI and cardiac
surgery
 Can coexist with acute pericarditis and chronic
constrictive disease

29. Causes
 Major causes---Tbc
 Neoplastic disease
 Gradual accumulation of fluid (chronic) permits
progressive stretching of pericardium
 Patient may develop a substantial fluid without
significant increase in intrapericardial pressure
 Rapid accumulation of fluid (acute) leads to
critical elevation of intrapericardial pressure

30. Investigations and clinical signs
 Clinical examination – SOB, orthopnoea,
tachycardia (varying degrees)
 Auscultation – may have muffled heart sounds
 ECG may show low amplitude QRS complexes and
alternating axis
 CXR – globular appearance to heart and therefore
increased cardiothoracic ratio
 Echo – size of effusion and haemodynamic effect
of it

31. Pericardial effusion

32. Echocardiography

33. Treatment
 Depends on the cause and nature
 If acute the cause is treated and the patient monitored
 If persistent problem or life threatening more dramatic
action is called for

35. Cardiac tamponade
(complication of pericardial effusion)
 This is a clinical diagnosis
- It is based upon the patient’s symptoms
 Investigations may be performed to confirm the
suspected cause of the symptoms (pericardial
effusion).

36.  Occurs when the fluid accumulation around the
heart impairs filling to such an extent that there is
haemodynamic compromise.
 It is a medical emergency and must be treated
promptly.
 Risk of death depends upon speed of diagnosis,
treatment and underlying cause of the tamponade.
 Depends on rate of accumulation and compliance
of the pericardium
 150ml that accumulated quickly could cause a
problem
 1000ml that accumulates very slowly may be
tolerated fairly well

37. Signs and symptoms
 Acutely unwell
 Significant SOB, rapid breathing
 Tachycardia
 Orthopnoea
 Cold, clammy extremities because of poor perfusion
 Kussmauls sign
 Pulsus paradoxus

38. Extra information
 Sharp chest pain worse on deep inspiration
 No added heart valve murmurs, pericardial friction
rub
 Elevated JVP

39. Investigations (used to confirm
only)
 CXR – ‘globular’ heart
 ECG (findings are suggestive not diagnostic)
- Sinus tachycardia
- Low voltage QRS complexes
- Electrical alternans (not always)
 Echo
- Size and location of effusion
- Any evidence of diastolic collapse
- ‘Swinging’ of the heart
- Decrease of insp. flow across MV

40. Treatment
 Medical emergency – intensive care environment
needed.
 Oxygen
 Volume expansion
 Bed rest with leg elevation
 Inotropic drugs if necessary

41. Pericardiocentesis
 Pericardiocentesis is the definitive therapy to remove
the excessive fluid
 Commonly performed in the cath lab but may be done
‘blind’ in an intensive care environment
 Treatment of underlying causes

42. Thank you