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


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

II. AUTOIMMUNE DISORDERS
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.

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

IV. RADIATION PERICARDITIS
V. RENAL FAILURE (uremia)
VI. TRAUMATIC CARDIAC INJURY
1. Penetrating - stab wound, bullet wound
2. Blunt non-penetrating - automobile steering wheel accident
VII. IDIOPATHIC

Pathogenesis

1) Vasodilation:
 transudation of fluid

2) Increased vascular permeability
 leakage of protein

3) Leukocyte exudation
neutrophils and mononuclear cells


Pathology
depends on underlying cause and severity of inflammation

serous pericarditis
serofibrinous pericarditis
suppurative (purulent) pericarditis
hemorrhagic pericarditis

Clinical Features of Acute Pericarditis

Idiopathic/viral
* 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
Pericardiocentesis:
low diagnostic yield
done therapeutically

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

Pericardial Effusion
Normal 15-50 ml of fluid
ETIOLOGY
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.


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)

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
EKG:
low voltage
“electrical alternans”
Echocardiogram
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

Tamponade-- Clinical Features
Symptoms:
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

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

 IPP
 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
Echocardiography
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
2) Timing - PRESYSTOLIC
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)

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

Tamponade -- Treatment
Pericardiocentesis
Pericardial Window
Balloon Pericardiotomy
Pre-pericardiocentisis
Post-pericardiocentesis
Constrictive Pericarditis
Late complication of pericardial disease
Fibrous scar formation
Fusion of pericardial layers
Calcification further stiffens pericardium
Etiologies:

Pathophysiology
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
ascites
peripheral edema
Physical exam
Kussmaul’s sign
Diagnosis
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
TAMPONADE
Low cardiac output state
JVD present
NO Kussmaul’s sign
Equalized diastolic pressures
RA: blunted y descent
Decreased heart sounds

CONSTRICTION

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

Pericardiocentesis
CONSTRICTION
Pulsus paradoxus:
Absent
Echo/MRI:
Normal systolic function
No effusion
Pericardial thickening
Treatment:
Pericardial stripping

Pathophysiology of Pericardial Disease.ppt