Pericardium 2

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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

Pericardium 2

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