20 February 2010

Pathophysiology of Pericardial Disease

Pathophysiology of Pericardial Disease

Pericardium - Anatomy

Normal pericardium is a fibro-serous sac which surrounds the heart and adjoining portions of the great vessels.
The inner visceral layer, also known as the epicardium, consists of a thin layer of mesothelial cells closely adherent to the surface of the heart. The epicardium is reflected onto the surface of the outer fibrous layer with which it forms the parietal pericardium.
The parietal pericardium consists of collagenous fibrous tissue and elastic fibrils.
Between the two layers lies the pericardial space, which contains approximately 10-50ml of fluid, which is an ultrafiltrate of plasma.
Drainage of pericardial fluid is via right lymphatic duct and thoracic duct.

Pericardial Layers:

Visceral layer
Parietal layer
Fibrous pericardium

Function of the Pericardium

1. Stabilization of the heart within the thoracic cavity by virtue of its ligamentous attachments -- limiting the heart’s motion.
2. Protection of the heart from mechanical trauma and infection from adjoining structures.
3. The pericardial fluid functions as a lubricant and decreases friction of cardiac surface during systole and diastole.
4. Prevention of excessive dilation of heart especially during sudden rise in intra-cardiac volume (e.g. acute aortic or mitral regurgitation).

Etiologies of Pericarditis

1. VIRAL - Coxsackie A and B, Influenza, adenovirus, HIV, etc.
2. BACTERIAL - Staphylococcus, pneumococcus, tuberculosis, etc.
3. FUNGAL - Candida
4. PARASITIC - Amoeba, candida, etc.

1. Systemic lupus erythematosus (SLE)
2. Drug-Induced lupus (e.g. Hydralazine, Procainamide)
3. Rheumatoid Arthritis
4. Post Cardiac Injury Syndromes i.e. postmyocardial Infarction (Dressler's) Syndrome, postcardiotomy syndrome, etc.

1. Primary mesothelioma
2. Secondary, metastatic
3. Direct extension from adjoining tumor

1. Penetrating - stab wound, bullet wound
2. Blunt non-penetrating - automobile steering wheel accident


1) Vasodilation:
 transudation of fluid

2) Increased vascular permeability
 leakage of protein

3) Leukocyte exudation
neutrophils and mononuclear cells

depends on underlying cause and severity of inflammation

serous pericarditis
serofibrinous pericarditis
suppurative (purulent) pericarditis
hemorrhagic pericarditis

Clinical Features of Acute Pericarditis

* Pleuritic Chest pain
* Fever
* Pericardial Friction Rub
3 component:
a) atrial or pre-systolic component
b) ventricular systolic component (loudest)
c) ventricular diastolic component

* EKG: diffuse ST elevation
PR segment depression

Diagnostic Tests
Echocardiogram: Pericardial effusin
N.B.: absence does not rule out pericarditis
N.B.: Pericarditis is a clinical diagnosis, not an Echo diagnosis!

Blood tests: PPD, RF, ANA
Viral titers
Search for malignancy
low diagnostic yield
done therapeutically

Pain relief
analgesics and anti-inflammatory
Steroids for recurring pericarditis
Antibiotics/drainage for purulent pericarditis
Dialysis for uremic pericarditis
Neoplastic: XRT, chemotherapy

Pericardial Effusion
Normal 15-50 ml of fluid
1. Inflammation from infection, immunologic process.
2. Trauma causing bleeding in pericardial space.
3. Noninfectious conditions such as:
a. increase in pulmonary hydrostatic pressure e.g. congestive heart failure.
b. increase in capillary permeability e.g. hypothyroidism
c. decrease in plasma oncotic pressure e.g. cirrhosis.
4. Decreased drainage of pericardial fluid due to obstruction of thoracic duct as a result of malignancy or damage during surgery.

Effusion may be serous, serofibrinous, suppurative, chylous, or hemorrhagic depending on the etiology.
Viral effusions are usually serous or serofibrinous
Malignant effusions are usually hemorrhagic.

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)

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

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)

Diagnostic studies
CXR: “water bottle” shaped heart
low voltage
“electrical alternans”
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
peripheral edema

Tamponade-- Clinical Features
Acute: (trauma, LV rupture)
profound hypotension
Slow/Progressive large effusion (weeks)
Fatigue (CO)
muffled heart sounds
pulsus paradoxus

Pulsus Paradoxus
Intrapericardial pressure (IPP) tracks intrathoracic pressure.
negative intrathoracic pressure is transmitted to the pericardial space

 blood return to the right ventricle
 jugular venous and right atrial pressures
 right ventricular volume
 interventricular septum shifts towards the left ventricle
 left ventricular volume
 LV stroke volume
 blood pressure (<10mmHg is normal) during inspiration

Pulsus Paradoxus
Exaggeration of normal physiology
> 10 mm Hg drop in BP
with inspiration
Tamponade -- Diagnosis

EKG: low voltage, sinus tachycardia,

electrical alternans
pericardial effusion
(r/o other etiologies in dif dx)
RA and RV diastolic collapse

Right Heart Catheterization
Catheterization Findings:
Elevated RA and RV diastolic pressures
Equalized diastolic pressures
Blunted “y” descent in RA tracing
y descent: early diastolic filling (atrial emptying)
 BP and Pulsus paradoxus
Pericardial pressure = RA pressure

Jugular venous pressure waves

Normal JVP contours
(1) A-wave
1) results from ATRIAL contraction
3) Peak of the a-wave near S1
(2) V-wave

1) results from PASSIVE filling of the right atrium while the tricuspid valve is closed during ventricular systole (Remember the V-wave is a "V"ILLING WAVE)

2) Large V-waves on the left side of the heart may be seen with mitral regurgitation, atrial septal defect, ventricular septal defect. The v-wave in the jugular venous pulse reflects right atrial events. To see the v-wave on the left side of the heart Swan-Ganz monitoring is needed

3) timing - peaks just after S2

(3) X-descent

1) results from ATRIAL RELAXATION

2) timing - occurs during ventricular systole, at the same time as the carotid pulse occurs

(4) Y-descent

1) results from a FALL in right atrial pressure associated with opening of the tricuspid valve

2) timing - occurs during ventricular diastole

(5) Generalizations

1) the A-wave in a normal individual is always larger than the V-wave

2) the X-descent is MORE PROMINENT than the Y-descent
RA Pressure Tracing

a wave: atrial contraction
v wave: passive filling of atria during
ventricular systole with mv/tv closed
y descent: early atrial emptying with mv/tv
open (early passive filling of ventricle)

blunted y descent (impaired rapid ventricular filling due to compression by high pericardial pressure)

Tamponade -- Treatment
Pericardial Window
Balloon Pericardiotomy
Constrictive Pericarditis
Late complication of pericardial disease
Fibrous scar formation
Fusion of pericardial layers
Calcification further stiffens pericardium

Rigid, scarred pericardium encircles heart:

Systolic contraction normal
Inhibits diastolic filling of both ventricles

 SV venous pressures
 CO systemic pulmonary congestion
Hypotension/shock JVD rales
Reflex tachycardia hepatomegaly
peripheral edema
Physical exam
Kussmaul’s sign
CXR: calcified cardiac silhouette
EKG: non-specific
CT or MRI: pericardial thickening

Cardiac Catheterization
Prominent y descent: “dip and plateau”:
rapid atrial emptying rapid ventricular filling then abrupt cessation of blood flow due to rigid pericardium

Elevated and equalized diastolic pressures (RA=RVEDP=PAD=PCW)
Constriction vs. Restriction

Similar presentation and physiology, important to differentiate as

constriction is treatable by pericardiectomy

Majority of diseases causing restriction are not treatable
Constrictive Pericarditis
Low cardiac output state
JVD present
NO Kussmaul’s sign
Equalized diastolic pressures
RA: blunted y descent
Decreased heart sounds


Low cardiac output state
JVD present
Kussmaul’s sign
Equalized diastolic pressures
RA: rapid y descent
Pericardial “knock”
Constriction vs. Tamponade Summary
Pulsus paradoxus:
Normal systolic function
Large effusion
RA & RV compression

Pulsus paradoxus:
Normal systolic function
No effusion
Pericardial thickening
Pericardial stripping

Pathophysiology of Pericardial Disease.ppt


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