Pericardial Disease

General Principles

Anatomy

• Two-layered (parietal & visceral) tissue sac surrounding heart & proximal great vessels Disease states

• Inflammation (w/ or w/o fluid accumulation) pericarditis

• Fluid accumulation (usually In setting of inflammation) effusion or tamponade

• Change in compliance (sequela of inflammation) — constriction

Pericarditis and Pericardial Effusion

Etiologies of Pericarditis

Infectious

(50%)

Viral: coxsackievirus, echovirus. adenovirus. EBV.VZV. HIV Bacterial (from endocarditis, pneumonia, or s/p cardiac surgery): S. pneumococcus, N. meningitidis, S. aureus Tuberculous (extension from lung or hematogenous); Lyme disease Fungal: Histo. Coccidio, Candida; Protozoal: Entamoeba. Echino

Neoplastic

(35%)

Common: metastatic (lung, breast, lymphoma, leukemia, renal cell) Rare: primary cardiac & serosal tumors (mesothelioma)

Autoimmune

Connective tissue diseases (SLE. RA. scleroderma. Sjogren's) Vasculitides (PAN. Churg-Strauss.Wegener's) Drug-induced (procainamide, hydralazine. INH. CsA)

Uremia

Develops in 20% of Pts, especially if on HD. May be transudative.

Cardiovascular

Acute transmural Ml (5-20%) Late post-MI (Dressler's syndrome) Proximal aortic dissection (up to 45%) Chest trauma or s/p cardiac procedure / surgery Postirradiation (>4000 cGy to mediastinum; may be acute or delayed; may be transudative)

Idiopathic

Most presumed to be undx viral

Effusions w/o pericarditis

CHF, cirrhosis, nephrotic syndrome, hypothyroidism, amyloidosis. Transudative.

(Loncet 2004:363:717)

(Loncet 2004:363:717)

Clinical manifestations {NEJM 2004:351:219S)

• Pericarditis: chest pain that is pleuritic, positional (i by sitting forward), radiates to trapezius; may be absent in tuberculous, neoplastic. post-XRT, and uremic pericarditis; ± fever; ± s/s of systemic etiologies

• Effusion: ranges from asymptomatic to tamponade (see below)

Physical exam

• Pericarditis: multiphasic friction rub (leathery sound w/ up to 3 components: atrial contraction, ventricular contraction, ventricular relaxation) that is notoriously variable and evanescent

• Effusion: distant heart sounds, dullness over left posterior lung field due to compressive atelectasis from pericardial effusion (Ewart's sign). PMI not displaced (in contrast to DCMP) Diagnostic studies (ehj 2004:25:587)

• ECG: may show evidence of pericarditis wI diffuse STE (concove up), PR depress..TWI;

classically and in contrast to STEMI.TWI do not occur until ST segments normalize; may show evidence of large effusion w/ low voltage and electrical alternans

• CXR: large effusion (>250 cc of fluid) -» cardiomegaly w/"water-botde" heart and epicardial halo

• Echocardiogram: presence, size. & location of effusion; presence of tamponade physiology, pericarditis itself w/o spec. abnl. although can sec pericardial stranding (fibrin or tumor) can also detect asx myocarditis

• CT will reveal pericardial effusions, often appearing larger than on echocardiography

• CK-MB or troponin (© in 30%. jacc 2003:42.2144) if myopericarditis

Workup for effusion

• r/o infxn: usually apparent from Hx & CXR; ? / acute and convalescent serologies | • r/o noninfectious etiologies: BUN. Cr. ANA. RF. screen for common malignancies

• Pericardiocentesis if suspect infxn or malignancy or if effusion large (>2 cm)

✓ cell counts.TP. LDH. glc. gram stain & Cx. AFB. cytology ADA. PCR for MTb. and specific tumor markers as indicated by clinical suspicion •'exudate" criteria:TP -3g/dl.TP'«fTP^ •0.5.LDHt«/LDHl<™ 0.6. or glc • 60 mg/dl high Se ( 90%) but very low Sp ( 20%); overall low utility (Own 1997;1111213)

• Pericardial bx if suspicion remains for malignancy or tuberculosis

Treatment of pericarditis

1 • NSAIDs (eg. ibuprofen 600-800 mg tid) • colchicine 0.5 mg bid (Ore 2005:112:2012) sx usually subside in 1-3 d. continue Rx for 7-14 d uama 2003:289:1150)

• Steroids (usually systemic; occasionally intrapericardial) for systemic autoimmune disorder, uremic, or refractory idiopathic disease

• Avoid anticoagulants

• Infectious effusion — pericardial drainage (preferably surgically) - systemic antibiotics

• Acute idiopathic effusion self-limited in 70-90% of cases

• Recurrent effusion — consider pericardial window (percutaneous vs. surgical)

Pericardial Tamponade

Etiology

• Any cause of pericarditis but especially malignancy, uremia, idiopathic.

proximal aortic dissection with rupture, myocardial rupture

• Rapidly accumulating effusions most likely to cause tamponade as no time for pericardium to stretch (T compliance) and accommodate fluid

Pathophysiology (N£/m 2003:3*9*84)

• ' intrapericardial pressure, compression of heart chambers, i venous return --»1 CO

• Diastolic pressures t & equalize in all cardiac chambers -» minimal flow of blood from

RA to RV when TV opens — blunted y descent

• Pulsus paradoxus (pathologic exaggeration of normal physiology)

Inspiration i intrapericardial & RA pressures -* t venous return -» t RV size septal shift to left Also, t pulmonary vascular compliance - ► I pulm venous return. Result is i LV filling -» I LV stroke volume & blood pressure Defined by respirophasic A SBP --10 mmHg due to i ventricular interdependence

Clinical manifestations

• Cardiogenic shock (hypotension, fatigue) without pulmonary edema

• Dyspnea may be due to t respiratory drive to augment venous return

Physical exam

• Beck's triad: distant heart sounds.' JVP. hypotension

• Hypotension (50%; occasionally hypertensive), reflex tachycardia, cool extremities

• Pulsus paradoxus (>75%) - I SBP -10 mmHg during inspiration

Ddx PE. hypovolemia, severe obstructive lung disease, constriction ( 1/3)

• i JVP with blunted y descent

• Distant heart sounds. - pericardial friction rub (30%)

• Tachypnea but clear lungs Diagnostic studies

• ECG: low voltage, electrical alternans. signs of pericarditis

• Echocardiogram: effusion. IVC plethora, septal shift with inspiration.

diastolic collapse of RA (Se 85%. Sp 80%) and/or RV (Se 80%. Sp 90%) respirophasic A's in transvalvular velocities (T across TV & i across MV w/ inspir.) postsurgical tamponade may be localized and not easily visible

• Cardiac cath (right heart and pericardial): elevation (15-30) and equalization of intrapericardial and diastolic pressures (RA. RV. PCWP). blunted y descent in RA ' in stroke volume postpericardiocentesis ultimate proof of tamponade if RA pressure remains elevated after drainage. Pt may have effuso-constrictive disease (NE/M 2004:350.469) or myocardial dysfxn (eg. from concomitant myocarditis)

Treatment

• Volume (but be careful as overfilling can worsen tamponade) and f inotropes

• Pericardiocentesis (except if due to aortic or myocardial rupture, in which cases consider removing just enough fluid to reverse PEA while awaiting surgery)

Constrictive Pericarditis

Etiology

• Any cause of pericarditis but especially postviral. radiation, uremia. TB. postcardiac surgery, and idiopathic

Pathophysiology

• Rigid pericardium limits diastolic filling 1 systemic venous pressures

• Venous return is limited only after early rapid filling phase; rapid i in RA pressure with atrial relaxation and opening of tricuspid valve and prominent x and y descents

• Kussmaul's sign: * JVP with inspiration (T venous return with inspiration but negative intrathoracic pressure not transmitted to heart because of rigid pericardium) Clinical manifestations

• Right-sided • left-sided heart failure Physical exam

• i JVP with prominent y descent, • Kussmaul's sign (Ddx: TS. acute cor pulmonale.

RV infarct. RCMP)

• Hepatomegaly, ascites, peripheral edema

• PMI usually not palpable, pericardial knock, usually no pulsus paradoxus

Diagnostic studies

• ECG: nonspecific

• CXR: calcification (MTb most common cause), especially in lateral view (although does not necessarily constriction)

• Echocardiogram: - thickened pericardium, "septal bounce" abrupt displacement of septum during rapid filling in early diastole

• Cardiac catheterization atria: Ms or Ws (prominent * and y descents)

ventricles: dip-and-plateau or square-root sign (rapid i pressure at onset of diastole, rapid t to early plateau) discordance between LV & RV pressure peaks during respiratory cycle (Ore 199633:2007)

• CT or MRI: thickened pericardium with tethering

Treatment

• Diuresis for intravascular volume overload, surgical pericardiectomy

Constrictive Pericarditis vs. Restrictive Cardiomyopathy

Evaluation

Constrictive pericarditis

Restrictive cardiomyopathy

Physical exam

® Kussmaul's sign Absent PMI 5 pericardial knock

* Kussmaul's sign Powerful PMI. r Sj and S< ± Regurgitant murmurs of MR,TR

ECG

± Conduction abnormalities

Echocardiogram

Normal wall thickness Septal bounce during early diastole

Inspiration t flow across TV and I flow across MV

* t wall thickness Biatrial enlargement

Inspiration -» 1 flow across TV & MV Slower peak filling rate Longer time to peak filling rate

CT/MRI

Thickened pericardium with tethering

Normal pericardium

Cardiac catheterization

Endomyocardial biopsy

Prominent x and y descents Dip-and-plateau sign

LVEDP RVEDP ± LVEDP RVEDP (espec.with vol.) RVSP 50 mmHg RVSP -60 mmHg RVEDP >1/3 RVSP RVEDP < 1 /3 RVSP Discordance of LV and RV Concordance of LV and RV pressure pressure peaks during peaks during respiratory cycle respiratory cycle

Usually normal ± Specific etiology of RCMP

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