1) Anatomy of pericardium2) Overview of pericardial disease3) Etiology4) Clinical presentation5) Treatment

Normal amount of pericardial fluid: 15-50 cc

Two layers:Outer layer is the

parietal pericardium and consists of layers of fibrous and serous tissue

Inner layer is visceral pericardium and consists of serous tissue only

Fibroelastic sac consisting of 2 layersVisceral at

epicardial sideParietal at

mediastinal side

Pericardial fluid formed from ultrafiltrate of plasma

Acute Fibrinous Pericarditis Pericardial Effusion

Cardiac tamponade Recurrent Pericarditis Constrictive Pericarditis

0.1% of hospitalized patients

5% of patients admitted to Emergency Department for non-acute myocardial infarction chest pain

Exact incidence and prevalence are unknown

Diagnosed in 0.1% of hospitalized patients and 5% of patients admitted for non-acute MI chest pain

Observational study: 27.7 cases/100,000 population/year

Chest pain: anterior chest, sudden onset, pleuritic; may decrease in intensity when leans forward, may radiate to one or both trapezius ridges

Pericardial friction rub: most specific, heard best at LSB

EKG changes: new widespread ST elevation or PR depression

Pericardial effusion: absence of does not exclude diagnosis of pericarditis

Supporting signs/symptoms: Elevated ESR, CRP Fever leukocytosis

1) Chest pain Sudden onset localized to anterior chest wall pleuritic sharp Positional: may improve if pt leans forward, worse

with lying flat2) Cardiac auscultation: Pericardial friction

rub Present in up to 85% of pts with pericarditis

without effusion friction of the two inflamed layers of pericardium,

typically triphasic rub, heard with diaphragm of stethoscope at left sternal border

3) Characteristic ECG changes4) Pericardial effusion

Stage 1: hours to daysDiffuse ST elevation

-sensitive v5-v6, I, II

ST depression I/aVRPR elevation aVRPR depression

diffuse -especially v5-v6PR change is marker

of atrial injury Stage 2:

Normalization

Stage 3:Diffuse T wave

inversionsST segments

isoelectric

Stage 4:EKG may

normalizeT wave

inversions may persist indefinitely

ST elevation in pericarditis Starts at J pointRarely exceeds 5mmRetains normal

concavityNon-localizing

Arrhythmias very unlikely in pericarditis (suggest myocarditis or MI)

51yo man with acute onset sharp substernal chest pain two days prior

Electrocardiogram in acute pericarditis showing diffuse upsloping ST segment elevations seen best here in leads II, III, aVF, and V2 to V6. There is also subtle PR segment deviation (positive in aVR, negative in most other leads). ST segment elevation is due to a ventricular current of injury associated with epicardial inflammation; similarly, the PR segment changes are due to an atrial current of injury which, in pericarditis, typically displaces the PR segment upward in lead aVR and downward in most other leads.

Small Moderate Large

LocationPosterior

Inferior to LVExtends to apex

Circumscribes heart

*Meas. @ Diastole <10 mm 10-15 mm >15 mm

*maximal width of pericardial stripe

Low voltage and Electric Alternans

Cardiomegaly due to a massive pericardial effusion. At least 200 mL of pericardial fluid must accumulate before the cardiac silhouette enlarges.

M-Mode

M-mode Cannot determine volume of accumulated fluid accurately

Aspirin NSAIDs Colchicine: can reduce or eliminate need for glucocorticoids Glucocorticoids: should be avoided unless required to treat

patients who fail NSAID and colchicine therapy Many believe that prednisone may perpetuate recurrences Intrapericardial glucocorticoid therapy: sx improvement and prevention

of recurrence in 90% of patients at 3 months and 84% at one year Other immunosuppression

Azothoprine (75-100 mg/day) Cyclophosphamide Mycophenolate: anecdotal evidence only Methotrexate: limited data IVIG: limited data

Pericardiectomy: To avoid poor wound healing, recommended to be off prednisone for one year. Reserved for the following cases: If >1 recurrence is accompanied by tamponade If recurrence is principally manifested by persistent pain despite an

intensive medical trial and evidence of serious glucocorticoid toxicity

Normal amt of pericardial fluid = 20-50 mL

Tamponade occurs when lg or rapidly formed effusions inc’d pressure in the pericardial space throughout the cardiac cycle

During inspiration, RV volume inc’s & in tamponade, the RV is unable to expand into the maximally stretched pericardium L-ward bulging of the interventricular septum dec’d LVEDV dec’d cardiac output & dec’d SBP during inspiration

Pressure in pericardium exceeds s Compressive effect in intrachamber Diagnostic techniques

2D looking for RA/RV collapse during diastoleM-mode for RA/RV collapse during diastoleDoppler of Mitral and Tricuspid inflow

Mitral inflow to decrease by 25% with inspiration Tricuspid inflow increased by 40% with inspiration

IVC diameter fails to increase with inspiration

HIV, bacterial (incl mycobacterial), viral, fungal CA - Esp lung, breast, Hodgkin’s, mesothelioma Radiation tx Meds - Hydralazine, Procainamide, INH, Minoxidil Post-MI (free wall ventricular rupture, Dressler’s syndrome) Connective tissue dzs – SLE, RA, Dermatomyositis Uremia Trauma Iatrogenic – (eg, from TLC / PA Cath / TV pacemaker insertion,

coronary dissection & perforation, sternal bx, pericardiocentesis, GE jnx surgeries)

Other - Pneumopericardium (d/t mech ventilation or gastropericardial fistula), Pleural effusions

Idiopathic

Sxs Chest Pain, dyspnea, near-syncope Generally more comfortable sitting forward Sxs c/w the underlying cause of tamponade

Physical Exam Beck’s Triad - Elev’d JVP, hypotension, dec’d heart

sounds JVP w/ preserved x descent and dampened or absent y

descent Generally w/ narrow pulse pressure

Tachycardia, other signs of HF (tachypnea, diaphoresis, cool extremities, cyanosis, etc)

Pulsus paradoxus Dec’d or absent cardiac impulse +/- Friction rub

Dec in SBP > 10-12 mmHg w/ inspiration

Can also occur in pts w/ COPD, pulm dz, PTX, severe asthma

Can have tamponade w/o pulsus paradoxus In pts w/ pre-existing

elev’s in diastolic pressures and/or volume (eg, LV dysfnx, AI and ASD)

Tamponade is a Clinical Diagnosis

Other Detection MethodsEKG

CXR

TTE

R Heart Cath

CT, MRI

Common Findings Sinus tachycardia Non-specific ST segment and T wave changes Changes assoc’d w/ acute pericarditis (incl diffuse STE &

PR depression)

Other Findings Dec’d voltage (non-specific and can also be d/t

emphysema, infiltrative myocardial dz, PTX, etc) Electrical alternans (specific but relatively insensitive for

lg effusions) 2/2 anterior-posterior swinging of the heart w/ each beat Best seen in leads V2 to V4

Combined P wave and QRS complex alternation (specific for cardiac tamponade)

Sudden inc in size of cardiac silhouette w/o specific chamber enlargement

Effacement of the normal cardiac borders

Development of a “flask” or “H2O-bottle” shaped heart

May have (+) fat pad sign Separation of mediastinal

/ retrosternal fat and epicardial fat by > 2 mm

Normal in patients with acute pericarditis unless pericardial effusion is present

Enlarged cardiac silhouette

Requires 200cc of fluid

If mild, can sometimes tx w/ medical mgmt Including 1 or more of the following:

NSAIDs, Colchcine, and/or steroids, depending on the suspected cause.

Require very close monitoring, including w/ serial TTEs and/or RHC

Most require urgent/emergent pericardiocentesis

Closed pericardiocentesis Generally in cath lab but can be at bedside Subxiphoid approach under echo guidance is

most common - minimizes risk & can assess completeness of fluid removal

Can alternatively use Fluoroscopic guidance Pigtail catheter often left in place

Open Pericardiocentesis in the OR May be best for loculated effusions, effusions

containing clots or fibrinous material, and/or effusions that are borderline in size

Allow for bx and creation of a pericardial window for recurrent effusions

Bedside pericardiocentesis if pt is in extremis

16- or 18-gauge needle inserted at angle of 30-45° to the skin, near the left xiphocostal angle, aiming toward the L shoulder