Pericardial Diseases

Front 1

Discuss the anatomy of the Pericardium:

Back 1

*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.

Front 2

What is the Function of the Pericardium?

Back 2

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).

Front 3

Big picture Etiologies of Pericarditis:
7 categories and a big huge list.

Back 3

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

Front 4

Pathogenesis and Pathology in Pericarditis:

Back 4

*Pathogenesis:
1) Vasodilation: transudation of fluid.
2) Increased vascular permeability from 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

Front 5

What are the Clinical Features of Acute Pericarditis?

Back 5

*Idiopathic/viral presents with:
1) Positional Pleuritic Chest pain (worse with inspiration).
2) Fever.
3) Pericardial Friction Rub:
-3 components:
a) atrial or pre-systolic component.
b) ventricular systolic component (loudest).
c) ventricular diastolic component.

*EKG shows diffuse ST elevation and PR segment depression.

Front 6

Back 6

EKG findings in Pericarditis
1) Note that the elevations are NOT LOCALIZED. Means this is not an MI.
2) Contour of the ST segment is upcoving (here, especially V2, V3, V4) in pericarditis. In an MI it is DOWNcoving.

Front 7

Discuss Diagnostic Tests for pericarditis:

Back 7

*Echocardiogram to look for Pericardial effusion.
-Note: absence does not rule out pericarditis
-Note: Pericarditis is a clinical diagnosis, not an Echo diagnosis!

*Blood tests: PPD, Rheumatoid Factor, ANA for SLE; Viral titers take days to come back. Blood tests are of limited usefulness.

*Search for malignancy.

*Pericardiocentesis:
-low diagnostic yield.
-done therapeutically.

Front 8

Discuss treatment for pericarditis:

Back 8

Pain relief with analgesics and anti-inflammatory drugs:
-ASA/NSAID’s.

*Steroids for recurring pericarditis.

*Antibiotics/drainage for purulent pericarditis.

*Dialysis for uremic pericarditis.

*Neoplastic: XRT, chemotherapy.

*Treat the underlying cause!

Front 9

Etiologies of Pericardial Effusion: 4

Back 9

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. CHF.
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.

Front 10

Pathophysiology of Pericardial Effusions:

Back 10

*Pericardium is relatively stiff.

*Symptoms of cardiac compression are dependant on:
1. Volume of fluid.
2. Rate of fluid accumulation.
3. Compliance characteristics of the pericardium.

Graphs:
A. Sudden increase of small amount of fluid (e.g. trauma)
B. Slow accumulation of large amount of fluid (e.g. CHF).

Front 11

Clinical features of pericardial effusions:

Back 11

*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:

1) dysphagia (compression of esophagus).
2) hoarseness (recurrent laryngeal nerve compression).
3) hiccups (diaphragmatic stimulation).
4) dyspnea (pleural inflammation/effusion).

Front 12

Describe the Physical Findings in pericardial effusion:

Back 12

*Muffled heart sounds

*Paradoxically reduced intensity of rub

*Ewart's sign (won't be on test): Compression of lung leading to an area of consolidation in the left infrascapular region (atalectasis, detected as dullness to percussion and bronchial breathing).

Front 13

Diagnostic studies for pericardial effusion:
what do you see on CXR?
what do you see on EKG?
what do you see on echo?

Back 13

*CXR: “water bottle” shaped heart.

*EKG:
1) low voltage.
2) “electrical alternans” (small and large QRSs).

*Echocardiogram shows fluid ("PE").

Front 14

Back 14

*Cardiac Tamponade!

*Fluid under high pressure compresses the cardiac chambers:
1) acutely: trauma, LV rupture – may not be very large.
2) gradually: large effusion, due to any etiology of acute pericarditis.

Front 15

Pathophysiology of Cardiac Tamponade:

Back 15

Front 16

Discuss Pulsus Paradoxus in Tamponade:

Back 16

*An exaggeration of the normal physiological response to inspiration.

Front 17

Tamponade-- Clinical Features:

Back 17

Front 18

How big is the BP drop in pulsus paradoxus?

Back 18

*Exaggeration of normal physiology.
>10 mm Hg drop in BP with inspiration.

*Right shows arterial line pressure. Note how LV and RV pressures are interdependent on each other.

Front 19

How is tamponade diagnosed?

Back 19

*EKG: low voltage, sinus tachycardia, electrical alternans.

*Echocardiography:
1) pericardial effusion (r/o other etiologies in dif dx).
2) RA and RV diastolic collapse.

Front 20

What are the Right Heart Catheterization findings in tamponade?

Back 20

*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.

Front 21

What are the normal contours of the Jugular venous pressure waves?

Back 21

(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.

Front 22

What does the RA pressure tracing look like in cardiac tamponade?

Back 22

*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).

Front 23

Back 23

*Pressure tracings in tamponade.
*Note that all of the diastolic pressures are about the same (~20), because the heart is being compressed in diastole. The pericardial pressure would be the same as well.

Front 24

How do pressure tracings change when tamponade is treated?

Back 24

*Post shows NORMAL y descent.
*Systolic BP comes up.

Front 25

What is Constrictive Pericarditis? What causes it?

Back 25

*Late complication of pericardial disease.
*Fibrous scar formation.
*Fusion of pericardial layers.
*Calcification further stiffens pericardium.

*Etiologies:any cause of pericarditis:
idiopathic
post-surgery
tuberculosis
radiation
neoplasm

Front 26

Pathophysiology of constrictive pericarditis:

Back 26

Front 27

What are the Physical exam findings in constrictive pericarditis?

Back 27

*Increased HR, decreased BP.
*ascites, edema, hepatomegaly.

*early diastolic “knock”
-after S2, as filling blood knocks against the pericardium.
-sudden cessation of ventricular diastolic filling imposed by rigid pericardial sac.

*Kussmaul’s sign (a CLASSIC! and PARADOXICAL! finding).

Front 28

Discuss the Kussmaul's sign in constrictive pericarditis:

Back 28

Front 29

Diagnosis of constrictive pericarditis:
what do you see on CXR?
EKG?
CT/MRI?

Back 29

Front 30

What are the catheterization findings in constrictive pericarditis?

Back 30

*OPPOSITE of what you see in tamponade.

Front 31

Table of findings in RCM and Constrictive pericarditis:

Back 31

*Similar presentation and physiology, important to differentiate, since constriction is treatable by pericardiectomy.
*Majority of diseases causing restriction are not treatable.
*Don't have to know this.

Front 32

Summary points of key difference I need to know between tamponade and constriction:

Back 32

*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.”

*IMPORTANT SLIDE*

Front 33

Key differences b/t tamponade and constriction:
pulsus?
echo findings?
treatment?

Back 33

*TAMPONADE:
-Pulsus paradoxus: Present

-Echo/MRI:
Normal systolic function
Large effusion
RA & RV compression

-Treatment: Pericardiocentesis (easy).


*CONSTRICTION:
-Pulsus paradoxus: Absent

-Echo/MRI:
Normal systolic function
No effusion
Pericardial thickening

-Treatment: Pericardial stripping (tough to do).