PERICARDIAL EFFUSION & TAMPONADE ... - Google Docs

PERICARDIAL​ ​EFFUSION​ ​&​ ​TAMPONADE

Mark​ ​Tuttle​ ​2017

ANATOMY​ ​AND​ ​PHYSIOLOGY  ● The​ ​pericardial​ ​sac​ ​normally​ ​contains​ ​15–35​ ​ml​ ​of​ ​serous​ ​fluid​ ​distributed​ ​mostly​ ​over​ ​the​ ​atrioventricular​ ​and​ ​interventricular grooves  ● As​ ​a​ ​result​ ​of​ ​its​ ​relatively​ ​inelastic​ ​physical​ ​properties,​ ​the​ ​pericardium​ ​limits​ ​acute​ ​cardiac​ ​dilatation​ ​and​ ​enhances mechanical​ ​interactions​ ​of​ ​the​ ​cardiac​ ​chambers ● The​ ​hemodynamic​ ​importance​ ​of​ ​a​ ​pericardial​ ​effusions​ ​is​ ​determined​ ​by​ ​the​ ​rate​ ​of​ ​fluid​ ​accumulation​ ​and​ ​overall​ ​fluid volume o Chronic​:​ ​Can​ ​accommodate​ ​>​ ​1​ ​L​ ​of​ ​fluid​ ​without​ ​tamponade​ ​physiology o Acute​:​ ​As​ ​little​ ​as​ ​100-200ml​ ​of​ ​fluid​ ​can​ ​cause​ ​tamponade​ ​physiology CLASSIFICATION  ● In​ ​general​ ​pericardial​ ​effusions​ ​can​ ​be​ ​classified​ ​into​ ​the​ ​following​ ​types:​ ​transudate,​ ​exudates,​ ​hemopericardium, chylopericardium,​ ​pyopericardium​ ​(pus),​ ​pneumopericardium ETIOLOGY  ● The​ ​most​ ​common​ ​causes​ ​of​ ​moderate​ ​to​ ​large​ ​effusions​ ​in​ ​developed​ ​countries:​ ​idiopathic/viral​ ​(30-40%),​ ​iatrogenic​ ​(16%), malignancy​ ​(13%),​ ​post-MI​ ​(8%),​ ​uremia​ ​(6%),​ ​bacterial/MTB​ ​infection​ ​(6%),​ ​collagen​ ​vascular​ ​disease​ ​(5%),​ ​hypothyroidism (2%) ● Causes​ ​of​ ​hemodynamically​ ​significant​ ​pericardial​ ​effusions​ ​(dyspnea,​ ​tachycardia,​ ​tamponade)​ ​from​ ​a​ ​study​ ​of​ ​173​ ​patients with​ ​pericardicentesis​5 o Neoplastic:​ ​33%​ ​(20%​ ​new​ ​diagnosis​ ​of​ ​malignancy) o Chronic-idiopathic:​ ​14% o Acute​ ​pericarditis:​ ​12% o Traumatic:​ ​12% o Bacterial:​ ​4% ● In​ ​developing​ ​countries​ ​tuberculosis​ ​is​ ​the​ ​leading​ ​cause​ ​of​ ​pericardial​ ​effusion​ ​(up​ ​to​ ​60%​ ​of​ ​cases)  CLINICAL​ ​FEATURES:​ ​Highly​ ​variable​ ​and​ ​dependent​ ​on​ ​the​ ​speed​ ​of​ ​pericardial​ ​fluid​ ​accumulation  ● Classic​ ​symptoms​ ​include​ ​dyspnea​ ​progressing​ ​to​ ​orthopnea,​ ​and​ ​chest​ ​pain/fullness  ● Additional​ ​symptoms​ ​which​ ​can​ ​occur​ ​due​ ​to​ ​compression​ ​of​ ​local​ ​structures​ ​include: o Nausea​ ​(diaphragm) o Dysphagia​ ​(esophagus) o Hoarseness​ ​(recurrent​ ​laryngeal​ ​nerve) o Hiccups​ ​(phrenic​ ​nerve)  ● Beck’s​ ​triad​​ ​(late​ ​findings):​ ​hypotension,​ ​distended​ ​neck​ ​veins,​ ​muffled​ ​heart​ ​sounds  ● Elevated​ ​Pulsus​ ​Paradoxus:​ ​Patients​ ​with​ ​current​ ​or​ ​impending​ ​hemodynamic​ ​compromise​ ​have​ ​an​ ​exaggerated​ ​pulsus paradoxus​ ​(normally​ ​10​ ​mmHg​ ​in​ ​tamponade​ ​is​ ​due​ ​to​ ​exaggerated​ ​ventricular​ ​interdependence​ ​when​ ​overall volume​ ​of​ ​cardiac​ ​chambers​ ​becomes​ ​fixed​ ​and​ ​any​ ​change​ ​in​ ​the​ ​volume​ ​of​ ​one​ ​side​ ​of​ ​the​ ​heart​ ​causes​ ​the opposite​ ​changes​ ​in​ ​the​ ​other​ ​side  o To​ ​measure​ ​the​ ​pulsus,​ ​record​ ​the​ ​systolic​ ​pressure​ ​at​ ​which​ ​Korotkoff​ ​sounds​ ​are​ ​first​ ​audible​ ​only​ ​during​ ​expiration and​ ​the​ ​systolic​ ​pressure​ ​at​ ​which​ ​they​ ​are​ ​audible​ ​through​ ​the​ ​whole​ ​respiratory​ ​cycle  ● Depending​ ​on​ ​the​ ​etiology​ ​of​ ​the​ ​pericardial​ ​effusion;​ ​fever,​ ​chills​ ​or​ ​evidence​ ​of​ ​malignancy​ ​may​ ​be​ ​present  DIAGNOSIS  ● EKG​:​ ​Low-voltage​ ​(20mm ● CXR​:​ ​an​ ​enlarged,​ ​globular​ ​heart​ ​may​ ​be​ ​present​ ​if​ ​chronic ● Cardiac​ ​tamponade​​ ​should​ ​be​ ​diagnosed​ ​clinically​ ​through​ ​evaluation​ ​of​ ​jugular​ ​venous​ ​pressure,​ ​tachycardia,​ ​dyspnea,​ ​and paradoxical​ ​arterial​ ​pulse.​ ​Blood​ ​pressure​ ​may​ ​be​ ​normal,​ ​decreased,​ ​or​ ​even​ ​elevated.​ ​ ​Hypotension​ ​is​ ​a​ ​LATE​ ​finding. ● The​ ​diagnosis​ ​of​ ​cardiac​ ​tamponade​ ​can​ ​be​ ​confirmed​ ​by​ ​echocardiogram​ ​by​ ​observing​ ​the​ ​following​ ​findings:​ ​diastolic collapse​ ​of​ ​the​ ​RA,​ ​abnormal​ ​respiratory​ ​variations​ ​of​ ​LV​ ​and​ ​RV​ ​dimensions,​ ​abnormal​ ​respiratory​ ​variation​ ​of​ ​tricuspid​ ​and mitral​ ​velocity​ ​usually​ ​in​ ​combination​ ​of​ ​IVC​ ​prominence o Perhaps​ ​the​ ​most​ ​specific​ ​(100%)​ ​and​ ​sensitive​ ​(>90%)​ ​parameter​ ​is​ ​the​ ​duration​ ​of​ ​RA​ ​inversion​ ​as​ ​measured​ ​by

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PERICARDIAL​ ​EFFUSION​ ​&​ ​TAMPONADE

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Mark​ ​Tuttle​ ​2017

the​ ​RA​ ​inversion​ ​time​ ​index​ ​(duration​ ​of​ ​inversion/cardiac​ ​cycle​ ​length).​ ​The​ ​cutoff​ ​value​ ​for​ ​the​ ​aforementioned specificity​ ​and​ ​sensitivity​ ​is​ ​>0.34. The​ ​recommended​ ​diagnostic​ ​work​ ​up​ ​includes:  o Chest​ ​x-ray o Evaluation​ ​of​ ​tuberculosis​ ​risk​ ​factors o Thyroid​ ​function​ ​tests o ESR,​ ​CRP o Anti-nuclear​ ​antibodies o Pericardiocentesis​ ​if​ ​the​ ​effusion​ ​is​ ​large​ ​and​ ​unexplained​ ​or​ ​if​ ​there​ ​is​ ​a​ ​high​ ​suspicion​ ​for​ ​a​ ​malignant​ ​or​ ​purulent process o Consider​ ​pericardial​ ​biopsy​ ​if​ ​workup​ ​remains​ ​non-diagnostic Pericardial​ ​fluid​ ​analysis  o Light’s​ ​criteria​ ​not​ ​generally​ ​helpful​ ​since​ ​nearly​ ​all​ ​effusions​ ​are​ ​exudative ▪ Israeli​ ​study​ ​of​ ​120​ ​effusions​ ​showed​ ​118/120​ ​met​ ​Light’s​ ​criteria​ ​for​ ​exudate​6 o Appropriate​ ​studies​ ​include:​ ​cell​ ​count​ ​w/​ ​differential,​ ​specific​ ​gravity,​ ​LDH,​ ​total​ ​protein,​ ​glucose,​ ​cytology, Gram/fungal/AF​ ​staining,​ ​appropriate​ ​cultures   ▪ Exudative​ ​effusions​ ​have​ ​the​ ​following​ ​properties:​ ​specific​ ​gravity​ ​>1.015,​ ​fluid​ ​protein/serum​ ​protein​ ​>0.5, fluid​ ​LDH/serum​ ​LDH​ ​>0.6,   ▪ Rheumatoid​ ​and​ ​bacterial​ ​effusions​ ​tend​ ​to​ ​have​ ​the​ ​highest​ ​percentage​ ​of​ ​neutrophils.   ▪ Purulent​ ​effusions​ ​with​ ​positive​ ​cultures​ ​often​ ​have​ ​glucose​ ​levels​ ​​ ​12​ ​mmHg​ ​in​ ​a​ ​patient​ ​with​ ​a​ ​large​ ​pericardial​ ​effusion​ ​is​ ​98%​ ​sensitive,​ ​of​ ​83%​ ​specific,​ ​and​ ​a​ ​positive​ ​LR of​ ​5.9 ■ >​ ​10​ ​mmHg​ ​has​ ​a​ ​positive​ ​LR​ ​of​ ​3.3 ■ ​ ​25%​ ​with​ ​tidal​ ​inspiration. References  1. Little WC,​ ​Freeman GL. Pericardial​ ​disease. Circulation.​ ​2006;113:1622–32. 2. Imazio​ ​M.​ ​Contemporary​ ​management​ ​of​ ​pericardial​ ​diseases. Curr​ ​Opin​ ​Cardiol. 2012;27(3):308-317. 3. Imazio​ ​M,​ ​Adler​ ​Y.​ ​Management​ ​of​ ​pericardial​ ​effusion. Eur​ ​Heart​ ​J. 2013;34(16):1186-1197. 4. Spodick​ ​DH.​ ​Acute​ ​cardiac​ ​tamponade.​ ​N​ ​Engl​ ​J​ ​Med.​ ​2003;349(7):684-90. 5. Ben-horin​ ​S,​ ​Bank​ ​I,​ ​Guetta​ ​V,​ ​Livneh​ ​A.​ ​Large​ ​symptomatic​ ​pericardial​ ​effusion​ ​as​ ​the​ ​presentation​ ​of​ ​unrecognized​ ​cancer: a​ ​study​ ​in​ ​173​ ​consecutive​ ​patients​ ​undergoing​ ​pericardiocentesis.​ ​Medicine​ ​(Baltimore).​ ​2006;85(1):49-53. 6. Ben-horin​ ​S,​ ​Bank​ ​I,​ ​Shinfeld​ ​A,​ ​Kachel​ ​E,​ ​Guetta​ ​V,​ ​Livneh​ ​A.​ ​Diagnostic​ ​value​ ​of​ ​the​ ​biochemical​ ​composition​ ​of​ ​pericardial

MarkTuttleMD.com

PERICARDIAL​ ​EFFUSION​ ​&​ ​TAMPONADE

Mark​ ​Tuttle​ ​2017

effusions​ ​in​ ​patients​ ​undergoing​ ​pericardiocentesis.​ ​Am​ ​J​ ​Cardiol.​ ​2007;99(9):1294-7. 7. Otto​ ​CM.​ ​Textbook​ ​of​ ​Clinical​ ​Echocardiography,​ ​Expert​ ​Consult​ ​-​ ​Online​ ​and​ ​Print.​ ​Elsevier​ ​Health​ ​Sciences;​ ​2013. 8. Lang​ ​R,​ ​Goldstein​ ​SA,​ ​Kronzon​ ​I​ ​et​ ​al.​ ​ASE’s​ ​Comprehensive​ ​Echocardiography.​ ​Elsevier​ ​Health​ ​Sciences;​ ​2015.

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