Pocket Medicine

CARDIOLOGY

PERICARDIAL DISEASE

GENERAL PRINCIPLES

Anatomy

•  2-layered (parietal & visceral) tissue sac surrounding heart & proximal great vessels

Disease states

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

•  Fluid accumulation → effusion ± tamponade

•  Decrease in compliance (sequela of inflammation) → constrictive pericarditis

•  Tamponade and constriction characterized by increased ventricular interdependence

PERICARDITIS AND PERICARDIAL EFFUSION

Clinical manifestations (NEJM 2004;351:2195)

•  Pericarditis: retrosternal chest pain that is pleuritic, positional (↓ 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 asx to tamponade (see below)

Physical exam

•  Pericarditis: multiphasic friction rub best heard at LLSB w/ diaphragm of stethoscope. Notoriously variable and evanescent leathery sound w/ up to 3 components: atrial contraction, ventricular contraction, ventricular relaxation (NEJM 2012;367:e20).

•  Effusion: distant heart sounds, dullness over left posterior lung field due to compressive atelectasis from pericardial effusion (Ewart’s sign)

Diagnostic studies (EHJ 2004;25:587; Circ 2006;113:1622 & 2010;121:916)

•  ECG: may show diffuse STE (concave up) & PR depression (except in aVR: ST ↓ & PR ↑), TWI; classically and in contrast to STEMI, TWI do not occur until STs normalize

Stages: (I) STE & PR ↓; (II) ST & PR normalize; (III) diffuse TWI; (IV) Tw normalize

ECG may show evidence of large effusion w/ low voltage & electrical alternans (beat-to- beat Δ in QRS amplitude and/or axis due to swinging heart)

•  CXR: if large effusion (>250 mL of fluid) → ↑ cardiac silhouette w/ “water-bottle” heart and epicardial halo

•  Echocardiogram: presence, size, & location of effusion; presence of tamponade physiology; pericarditis itself w/o spec. abnl (∴ echo can be nl), although can see pericardial stranding (fibrin or tumor); can also detect LV/RV dysfxn (myocarditis ?)

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

•  CK-MB or troponin ( in ~30%, JACC 2003;42:2144) if myopericarditis. Consider CRP/ESR.

Workup for effusion

•  r/o infxn: usually apparent from Hx & CXR; ? value of ✓ acute and convalescent serologies

•  r/o noninfectious etiologies: BUN, Cr, ANA, RF, HIV, screen for common malignancies

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

✓ 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 >3 g/dL, TPeff/TPserum >0.5, LDHeff/LDHserum >0.6 or glc <60 mg/dL high Se (~90%) but very low Sp (~20%); overall low utility (Chest 1997;111:1213)

•  Pericardial bx if suspicion remains for malignancy or tuberculosis

Treatment of pericarditis (EHJ 2004;25:587; Circ 2006;113:1622)

•  NSAIDs (eg, ibuprofen 600–800 mg tid × 7–14 d then taper) ± colchicine 1–2 mg × 1 → 0.5–1 mg bid × 3 mo (Circ 2005;112:2012; Heart 2012;98:1078); sx usually subside in 1–3 d

•  Steroids (usually systemic; occ. intrapericardial) only for systemic rheum or autoimmune disorder, uremic, preg., contraindication to NSAID, or refractory idiopathic dis.

Systemic steroids appear to ↑ rate of pericarditis recurrence (Circ 2008;118:667).

•  Avoid anticoagulants

•  Infectious effusion → pericardial drainage (preferably surgically) + systemic antibiotics

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

•  Recurrent pericarditis (Circ 2007;115:2739)

risk factors: subacute, lg effusion/tamponade, T >38°C, lack of NSAID response after 7 d treatment: add colchicine 0.5–1 mg bid × 6 mo (Annals 2011;155:409)

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

PERICARDIAL TAMPONADE

Etiology

•  Any cause of pericarditis but esp. malignancyuremiaidiopathic, proximal aortic dissection with rupture, myocardial rupture

•  Rapidly accumulating effusions most likely to cause tamponade as no time for pericardium to stretch (eg, to ↑ compliance) and accommodate ↑ intrapericardial fluid volume

Pathophysiology (NEJM 2003;349:684)

•  ↑ intrapericardial pressure, compression of heart chambers, ↓ venous return → ↓ CO

•  Diastolic pressures ↑ & equalize in all cardiac chambers → minimal flow of blood from RA to RV when TV opens → blunted y descent

•  ↑ ventricular interdependence → pulsus paradoxus (pathologic exaggeration of nl physio)

Inspiration → ↓ intrapericardial & RA pressures → ↑ venous return → ↑ RV size → septal shift to left. Also, ↑ pulmonary vascular compliance → ↓ pulm venous return. Result is ↓ LV filling → ↓ LV stroke volume & blood pressure.

Clinical manifestations

•  Cardiogenic shock (hypotension, fatigue) without pulmonary edema

•  Dyspnea (seen in ~85%) may be due to ↑ respiratory drive to augment venous return

Physical exam ( JAMA 2007;297:1810)

•  Beck’s triad (present in minority of cases): distant heart sounds, ↑ JVPhypotension

•  ↑ JVP (76%) w/ blunted y descent

•  Reflex tachycardia (77%), hypotension (26%; occasionally hypertensive), cool extremities

•  Pulsus paradoxus (Se 82%, Sp 70%) = ↓ SBP ≥10 mmHg during inspiration

 LR 3.3 (5.9 if pulsus >12),  LR 0.03

Ddx = PE, hypovolemia, severe COPD, constriction (~13), RV infarct

Can be absent if pre-existing ↑ LVEDP, arrhythmia, severe AI, ASD, regional tamponade

•  Distant heart sounds (28%), ± pericardial friction rub (30%)

•  Tachypnea but clear lungs

Diagnostic studies

•  ECG: ↓ voltage (seen in 42%), electrical alternans (20%), ± signs of pericarditis

•  CXR: ↑ cardiac silhouette (89%)

•  Echocardiogram effusion, IVC plethora, septal shift with inspiration

diastolic collapse of RA (Se 85%, Sp 80%) and/or RV (Se <80%, Sp 90%)

respirophasic Δ’s in transvalvular velocities (↑ across TV & ↓ across MV w/ inspir.)

postsurgical tamponade may be localized and not easily visible

•  Cardiac cath (right heart and pericardial): elevation (15–30 mmHg) 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, may have effusive-constrictive disease (NEJM 2004;350:469) or myocardial dysfxn (eg, from concomitant myocarditis)

Treatment

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

•  Avoid vasoconstrictors as will ↓ stroke volume & potentially ↓ HR

•  Pericardiocentesis (except if due to aortic or myocardial rupture, in which case

consider removing just enough fluid to reverse PEA en route to emergent surgery)

CONSTRICTIVE PERICARDITIS

Etiology (Circ 2011;124:1270)

•  Any cause of pericarditis (~1–2% incidence overall after acute pericarditis)

•  Highest risk w/ TBbacterialneoplastic, connective tissue, postcardiac surgery

•  Viral/idiopathic, as most common cause of pericarditis, also account for signif proportion

Pathophysiology

•  Adhesion of visceral and parietal pericardial layers → rigid pericardium that limits diastolic filling of ventricles → ↑ systemic venous pressures

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

•  Kussmaul sign: JVP does not decrease with inspiration (↑ venous return with inspiration but negative intrathoracic pressure not transmitted to heart because of rigid pericardium)

Clinical manifestations (NEJM 2011;364:1350)

•  Right-sided > left-sided heart failure (systemic congestion > pulmonary congestion)

Physical exam

•  ↑ JVP with prominent y descent Kussmaul sign (Ddx: tricuspid stenosis, acute cor pulmonale, RV failure and RV infarct, RCMP)

•  Hepatosplenomegaly, ascites, peripheral edema. Consider on Ddx of idiopathic cirrhosis.

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

Diagnostic studies

•  ECG: nonspecific, AF common (up to 33%) in advanced cases

•  CXR: calcification (MTb most common), esp. in lateral view (although not specific)

•  Echocardiogram: ± thickened pericardium, “septal bounce” = abrupt displacement of septum during rapid filling in early diastole

•  Cardiac catheterization

atria: Ms or Ws (prominent x and y descents)

ventricles: dip-and-plateau or square-root sign (rapid ↓ pressure at onset of diastole, rapid ↑ to early plateau)

discordance between LV & RV pressure peaks during respiratory cycle (Circ 1996;93:2007)

•  CT or MRI: thickened pericardium (>4 mm; Se ~80%), w/ tethering (Circ 2011;123:e418)

Treatment

•  Diuresis for intravascular volume overload; surgical pericardiectomy in advanced cases

•  ? MRI able to predict reversibility with anti-inflammatory agents (Circ 2011;124:1830)