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Pathophysiology of Pericardial
DiseaseIMS 350
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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 thesurface 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, whichcontains approximately 10-50ml of fluid, which is an
ultrafiltrate of plasma.
Drainage of pericardial fluid is via right lymphatic duct and
thoracic duct.
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Pericardium: Anatomy
Pericardial Layers:
Visceral layer
Parietal layer
Fibrous pericardium
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Function of the Pericardium
1. Stabilization of the heart within the thoracic cavity by virtue of its
ligamentous attachments -- limiting the hearts 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).
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Etiologies of PericarditisI. 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 Arthritis4. 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 tumorIV. RADIATION PERICARDITIS
V. RENAL FAILURE (uremia)
VI. TRAUMATICCARDIAC INJURY
1. Penetrating - stab wound, bullet wound
2. Blunt non-penetrating - automobile steering wheel accident
VII. IDIOPATHIC
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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 inflammationserous pericarditis
serofibrinous pericarditis
suppurative (purulent) pericarditis
hemorrhagic pericarditis
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Clinical Features of Acute PericarditisIdiopathic/viral
* Pleuritic Chest pain
* Fever
* Pericardial Friction Rub
3 component:
a) atrial or pre-systolic componentb) ventricular systolic component (loudest)
c) ventricular diastolic component
* EKG: diffuse ST elevation
PR segment depression
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EKG findings in Pericarditis
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Diagnostic Tests
Echocardiogram: Pericardial effusion
N.B.: absence does not rule out pericarditis
N.B.: Pericarditis is a clinical diagnosis, not an Echo diagnosis!
Blood tests: PPD, RF, ANAViral titers
Search for malignancy
Pericardiocentesis:
low diagnostic yield
done therapeutically
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Treatment
Pain relief
analgesics and anti-inflammatory
ASA/NSAIDs
Steroids for recurring pericarditis
Antibiotics/drainage for purulent pericarditis
Dialysis for uremic pericarditis
Neoplastic: XRT, chemotherapy
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Pericardial EffusionNormal 15-50 ml of fluid
ETIOLOGY1. 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.
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Pathophysiology
Pericardium relatively stiffSymptoms 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)
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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)
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Physical FindingsPhysical 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 percussionand bronchial breathing)
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Diagnostic studies
CXR: water bottle shaped heart
EKG:
low voltage electrical alternans
Echocardiogram
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Cardiac TamponadeFluid 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
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CardiacTamponade -- Pathophysiology
Accumulation of fluid under high pressure:compresses cardiac chambers & impairs
diastolic filling ofboth ventricles
q SV ovenous pressures
q CO systemic pulmonary congestion
Hypotension/shock JVD rales
Reflex tachycardia hepatomegalyascites
peripheral edema
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Tamponade-- Clinical Features
Symptoms:Acute: (trauma, LV rupture)
profound hypotension
confusion/agitation
Slow/Progressive large effusion (weeks)
Fatigue (qCO)Dyspnea
JVD
Signs:
Tachycardia
Hypotension
rales/edema/ascites
muffled heart sounds
pulsus paradoxus
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Pulsus ParadoxusIntrapericardial pressure (IPP) tracks intrathoracic pressure.
Inspiration:
negative intrathoracic pressure is transmitted to the
pericardial space
q IPP
oblood return to the right ventricle
qjugular venous and right atrial pressures
o right ventricular volume interventricular septum
shifts towards the left ventricle
q left ventricular volume
q LV stroke volume
qblood pressure (
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Pulsus ParadoxusExaggeration of normal physiology
> 10 mm Hg drop in BP
with inspiration
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Tamponade -- DiagnosisEKG: low voltage, sinus tachycardia,
electrical alternans
Echocardiography
pericardial effusion
(r/o other etiologies in dif dx)
RA and RV diastolic collapse
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Right Heart Catheterization
Catheterization Findings:
Elevated RA and RV diastolic pressures
Equalized diastolic pressuresBlunted y descent in RA tracing
y descent: early diastolic filling (atrial emptying)
q BP and Pulsus paradoxus
Pericardial pressure = RA pressure
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Jugular venous pressureJugular venous pressure
waveswaves 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 thetricuspid 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-Ganzmonitoring 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 timeas the carotid pulse occurs
(4) Y-descent
1) results from a FALL in right atrial pressure associated withopening 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-
wave2) the X-descent is MORE PROMINENT than the Y-descent
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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 ventricularfilling due to compression by high
pericardial pressure)
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Tamponade
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Tamponade -- Treatment
Pericardiocentesis
Pericardial Window
Balloon Pericardiotomy
Pre-pericardiocentisis
Post-pericardiocentesis
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Constrictive Pericarditis
Late complication of pericardial disease
Fibrous scar formation
Fusion of pericardial layers
Calcification further stiffens pericardium
Etiologies:any cause of pericarditis
idiopathic
post-surgery
tuberculosisradiation
neoplasm
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Pathophysiology
Rigid, scarred pericardium encircles heart:
Systolic contraction normal
Inhibits diastolic filling ofboth ventricles
q SV ovenous pressures
q CO systemic pulmonary congestion
Hypotension/shock JVD rales
Reflex tachycardia hepatomegaly
ascites
peripheral edema
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Physical exam
oHR, qBP
ascites, edema, hepatomegaly
early diastolic knockafter S2
sudden cessation of ventricular diastolic filling imposed
by rigid pericardial sac
Kussmauls sign
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Kussmauls Sign
inspiration:q
intrathoracic pressure,o
venous return to thoraxqintrathoracic pressure not transmitted though to RV
no pulsus paradoxus!
no inspiratory augmentation of RV filling (rigid pericardium)
intrathoracic systemic veins become distended
JVP rises with inspiration (normally falls)
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Diagnosis
CXR: calcified cardiac silhouetteEKG: non-specific
CT or MRI: pericardial thickening
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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)
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Constriction vs. Restriction
Similar presentation and physiology, important to differentiate as
constriction is treatable by pericardiectomy
Majority of diseases causing restriction are not treatable
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Constrictive Pericarditis
Kussmauls
RV=LV,dip & plateau
Equalized diastolic pressures
Tachycardia, low voltage
Thickened pericardium
Thickened pericardium
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TAMPONADE
Low cardiac output state
JVD present
NO Kussmauls sign
Equalized diastolic
pressures RA: blunted y descent
Decreased heart sounds
CONSTRICTION
Low cardiac output state
JVD present
Kussmauls sign
Equalized diastolic
pressures RA: rapid y descent
Pericardial knock
Constriction vs. Tamponade
Summary
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Constriction vs. Tamponade
SummaryTAMPONADE
Pulsus paradoxus:
PresentEcho/MRI:
Normal systolic function
Large effusion
RA & RV compression
Treatment:
Pericardiocentesis
CONSTRICTION
Pulsus paradoxus:
AbsentEcho/MRI:
Normal systolic function
No effusion
Pericardial thickening
Treatment:
Pericardial stripping