Pericardial

disease
Tan Hong-Yong
Department of Diagnosis
Jining Medical College
What do you know about the
pericardium?
 What is it ?

 Where is it ?

 What is it’s function ?

What is it ?
 Double-walled fibrous sac that contains the
heart and the roots of the great vessels
 Serous membrane – two continuous
layers separated by a small amount of
fluid lubricant (10-20mls straw coloured)
 Layers are called visceral and parietal
 Visceral is inner layer (epicardium)
 Parietal is continuous with diaphragm and
outer walls of great arteries.
Where is it?
 Surrounds the heart
 Continuous with the great arteries and
the diaphragm.
What is it’s function ?

 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 (not the
case in chronic setting)
Learning Outcomes
 Outline the aetiology, prevalence and
mechanism of pericardial disease
 Describe the effects of the pathology on the
patient
 Identify investigations used in the diagnosis
 Explain how investigation results aid in
diagnosis
 Detail the treatment and prognosis of the
pericardial disease
Introduction
 Pericardial disease is potentially
curable
 Accounts for 7% of all hospitalizations
in Africa
 Spectrum of the disease is determined
by epidemiological setting of patient
 Western countries – largely idiopathic
 Developing countries – tuberculous
 But there are a large number of
diseases that can cause it.
Pericardial disease

 Acute pericarditis

 Pericardial effusion

 Constrictive pericarditis
Acute pericarditis
Etiology
 Inflammatory Pericarditis
 Infection caused by living agents
 Inflammation caused by noliving agents
 Uremic Pericarditis
 postmyocardial infarction or cardiac surgery
(Dressler’s syndrome)
 Radiation therapy
 Other pericarditis
• Collagen vascular
• myxedema
• Neoplastic disease (commonly lung or breast) –
6%
Viral Pericarditis

 The more common viral infections causing

pericarditis include coxsackievirus A and B,
echovirus, and adenovirus.
 HIV (Human Immunodeficiency Viruses) can
infect the pericardium or facilitate infection
by other organisms which are ordinarily not
virulent.
Tuberculous Pericarditis

 Incidence of pericarditis in patients with

pulmonary TB ranged from 1-8%.
 Physical findings: fever, pericardial friction
rub, hepatomegaly.
 TB skin test usually positive.
 Fluid smear for TB often negative.
 Pericardial biopsy more definitive.
Bacterial Pericarditis
 any bacteria may infect the pericardium, the
notable offenders are Staphylococcus,
Pneumococcus, Streptococcus (rheumatic
pancarditis).
 Less common bacteria can invade the
pericardium when the bacterial flora have
been altered by prolonged antibiotic use and
when the immune system is seriously
compromised.
Bacterial Pericarditis
 Rare condition in antibiotic era (steadily
decreased over last 40 years).
 Typically arises from contiguous spread of
intrathoracic infection (pneumonia,
endocarditis, trauma).
 Usually fatal without adequate treatment
 Diagnosis frequently missed.
 Often lacks characteristic features of acute
pericarditis.
Uremic Pericarditis

 occurring in 6 -10% of patients with

advanced renal failure who are not being
dialyzed.
 13% of patients on dialysis ( from both
inadequate dialysis and/or fluid overload).
 in uremic pericarditis, the electrocardiogram
does not usually show the typical diffuse ST
and T wave elevation.
Dressler’s Syndrome

 fever, pericarditis, pleuritis.

 typically with a low grade fever and a
pericardial friction rub.
 occurs in the first few days to several weeks
following MI or heart surgery.
 incidence of 6-25% .
 treat with high-dose aspirin.
Radiation Pericarditis
 Radiation exposure can cause acute
pericarditis soon after exposure, and late
pericardial effusion or constrictive
pericarditis.
 Most cases of radiation pericarditis are
secondary to therapy for Hodgkin's disease,
or bronchogenic or breast cancer.
Collagen vascular
disease
 Rheumatic diseases can involve the

pericardium: systemic lupus erythematosus

(SLE) and rheumatoid arthritis, progressive
systemic sclerosis, and mixed connective
tissue disease,etal.
Malignancy
 May be responsible for ~6% of cases of acute
pericardial disease.
 Metastatic involvement of the pericardium

most often reflects a primary in the breast,

lung, or lymph nodes.
 Primary tumors of the pericardium as highly

malignant mesothelioma.
 not easy to decide whether the pericardial

disease is a manifestation of the neoplasm

itself or of treatment by radiation or
Chemotherapy.
Metabolic Disorders

 Severe Hypothyroidism.
 ↓ cardiac contractility, mass, heart rate.
 ↑ peripheral vascular resistance.
 may cause of pericardial effusion but not
usually .
 Signs of cardiovascular dysfunction are not
common:
– Exertional dyspnea and exercise intolerance.
– Bradycardia.
– Hypertension (20-40%) .
– Cardiac dysfunction, with poor contractility,
dilatation or pericardial effusion.
– Edema.
 Patient may appear to have congestive heart
failure. However, heart failure due solely to
hypothyroidism is rare.
Pathology and
pathophysiology
Inflammation provokes
a fibrinous exudate with
or without serous
effusion.
The normal transparent
and glistening
pericardium is turned
into a dull, opaque, and
“sandy” sac.
Pathology and
pathophysiology
 It can cause
pericardial
scarring with
adhesions and
fibrosis-----
Constrictive
Pericarditis.
Pathophysiology
Pericardium relatively stiff
Symptoms of cardiac compression dependant on:
1. Volume of fluid
2. Rate of fluid accumulation
3. Compliance characteristics of the pericardium

A. Sudden increase of
small amount of fluid
(e.g. trauma)
B. Slow accumulation
of large amount of
fluid (e.g. CHF)
Cardiac Tamponade
Fluid under high pressure compresses the cardiac
chambers:
acute: trauma, LV rupture – may not be very large.
gradual: large effusion, due to any etiology of acute
pericarditis.
 CardiacTamponade --
Pathophysiology
Accumulation of fluid under high pressure:
compresses cardiac chambers & impairs
diastolic filling of both ventricles

↓ SV ↑venous pressures

↓ CO systemic pulmonary congestion

Hypotension/shock JVD rales

Reflex tachycardia hepatomegaly
ascites
peripheral edema
Clinical features
Small effusions do not produce hemodynamic
abnormalities.
Large effusions, in addition to causing hemodynamic
compromise, may lead to compression of adjoining
structures and produce symptoms of:
• dysphagia (compression of esophagus)
• hoarseness (recurrent laryngeal nerve
compression)
• hiccups (diaphragmatic stimulation)
• dyspnea (pleural inflammation/effusion)
Physical Findings
Physical Findings:
 Muffled heart sounds

 Paradoxically reduced intensity of rub

 Ewart's sign:

Compression of lung leading to an area of

consolidation in the left infrascapular region
(atalectasis, detected as dullness to percussion
and bronchial breathing).
CardiacTamponade
Symptoms: -- Clinical
Features
Acute: (trauma, LV rupture)
profound hypotension
confusion/agitation
Slow/Progressive large effusion (weeks)
Fatigue (↓CO)
Dyspnea
JVD
Signs:
Tachycardia
Hypotension
rales/edema/ascites
muffled heart sounds
pulsus paradoxus
 Raised jugular
venous
pressure.
Laboratory finding

 Chest x-ray
 ECG
 Echo
 Catheter laboratory investigations
 Chest x-ray
 CXR – globular
appearance to heart
and therefore
increased
cardiothoracic
ratio.
 “water bottle”
shaped heart.
ECG (acute pericarditis)
ECG differential diagnosis
- MI
 What leads is the ST elevation in?
 What shape is the elevation?
 Are there Q waves?
 Do the ST –T changes evolve with time?
 History of the patient.
 Cardiac enzymes etc.
Pericardial effusion
 EKG:
 low voltage
 “electrical
alternans”
Echocardiography

 Echo – size of
effusion and
haemodynamic
effect of it.
Catheter lab

diastolic
equalization
of left and
right heart
pressures
High RA
pressures
Diagnosis of pericarditis

 Patient will have 2 or more of the

following;
 Characteristic chest pain.
 Pericardial friction rub (auscultation).
 ECG showing characteristic ST elevation
(caused by epicardial injury).
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
Treatment
Patients require bed rest.
Pain relief
NSAID (aspirin, indomethacin) are generally
accepted as effective for relieving symptoms
of chest pain.
Antibiotics/drainage for particular infectious
pericarditis.
Dialysis for uremic pericarditis.
Neoplastic: x-ray radiation treatment(XRT),
chemotherapy.
Treatment-- Cardiac
Tamponade
 Give oxygen.
 monitor ECG and BP.
 Elevate legs.
 Consider volume expansion.
 Seek expert help.
 Consider moving to an intensive care
environment.
 Urgent echo.
 Assess need for Pericardiocentesis.
Prognosis
 Pericarditis is usually a benign disorder.
 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.
 Chronic
constrictive
pericarditis
Causes

 Tuberculous constrictive pericarditis was

common cause of constriction pre 1960 –
decline in incidence nowdays.
 Post-radiotherapy constriction features
prominently today along with post-
surgical causes.
 Needs to be differentiated from restrictive
cardiomyopathy when making diagnosis.
Physical exam

• ↑HR, ↓BP
• ascites, edema, hepatomegaly
• early diastolic “knock” after S2
• sudden cessation of ventricular diastolic filling
imposed by rigid pericardial sac
• Kussmaul’s sign
Kussmauls sign

 Normal subjects – inspiration causes a

decrease in chest pressure. Increase in
venous return – jugular venous
pressure(JVP) falls
 Constrictive pericarditis – Increased venous
return cannot be accommodated in RV
because of high EDP
 So JVP rises on inspiration
Investigations
As for acute pericarditis;
 Clinical examination – prime symptoms likely
to be RHF and shortness of breath.
 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.
Chest x-ray

 Occasionally
calcification noted
 More useful to
determine whether
there is a coexisting
effusion (fluid
accumulation)
Echo findings
 Thick pericardium and small chambers.
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.