wednesday morning conference december 14 th 2005 kenneth saland m.d. facc

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Wednesday Morning Wednesday Morning Conference Conference December 14 December 14 th th 2005 2005 Kenneth Saland M.D. FACC Kenneth Saland M.D. FACC

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Page 1: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Wednesday Morning ConferenceWednesday Morning ConferenceDecember 14December 14thth 2005 2005

Kenneth Saland M.D. FACCKenneth Saland M.D. FACC

Page 2: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Case PresentationCase Presentation 43 y/o white man43 y/o white man

Chief complaint(s)Chief complaint(s)

Intermittant abdominal painIntermittant abdominal pain

BloatingBloating

Page 3: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

History of present illnessHistory of present illness

3 mos of abdominal pain-intermittent3 mos of abdominal pain-intermittent

BloatingBloating

Loose bowel movements Loose bowel movements

More recently swelling in lower extremitiesMore recently swelling in lower extremities

Weight loss of 20 lbsWeight loss of 20 lbs

Page 4: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

PMHPMH BPHBPH

AllergyAllergy NoneNone

SHSH No tobacco, married, 1 daughter a/wNo tobacco, married, 1 daughter a/w No IVDANo IVDA Anabolic steroids in early 1990’s Anabolic steroids in early 1990’s Drinks 2-3 alcoholic drinks per monthDrinks 2-3 alcoholic drinks per month Busy engineerBusy engineer

Page 5: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

PSHPSH Nasal surgeryNasal surgery Squamous ca lesion removed rt shoulder 1980Squamous ca lesion removed rt shoulder 1980

MedsMeds NoneNone

FHFH Both parents deceasedBoth parents deceased Mother with breast CA, father had duodenal CAMother with breast CA, father had duodenal CA No cardiac historyNo cardiac history

Page 6: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Review of SystemsReview of Systems

Wt loss, fatigue, poor appetiteWt loss, fatigue, poor appetite

Dyspnea on exertionDyspnea on exertion

No chest pain No chest pain

Palpitations intermittantlyPalpitations intermittantly

Loose stoolsLoose stools

Page 7: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Physical ExamPhysical Exam

Bp 120/60 HR 100 regular RR-22 sat 98% RABp 120/60 HR 100 regular RR-22 sat 98% RA

Wt 100 kg Height 6’3”Wt 100 kg Height 6’3”

Marked JVD Marked JVD

Clear lungsClear lungs

Tachycardic, regular no murmursTachycardic, regular no murmurs

Page 8: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

AbdomenAbdomen

Mild generalized tendernessMild generalized tenderness

Positive bowel sounds Positive bowel sounds

No hepatosplenomegaly notedNo hepatosplenomegaly noted

Distended and edematousDistended and edematous

Page 9: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Extremities –trace peripheral edemaExtremities –trace peripheral edema Neuro-grossly normalNeuro-grossly normal

EKG: atrial flutter with rate of 100EKG: atrial flutter with rate of 100

CXR-normal heart size, clear lung fieldsCXR-normal heart size, clear lung fields

Page 10: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

LabsLabs wbc-5.7wbc-5.7

Hgb-12 Hgb-12

Platelets-257Platelets-257

Cr-1.0 Na 141 K 4.5 CO2 26 Ca 9.6 Cr-1.0 Na 141 K 4.5 CO2 26 Ca 9.6

Albumin 4.2, INR 1.3 AST 16 ALT 12 AP 94 total bilirubinAlbumin 4.2, INR 1.3 AST 16 ALT 12 AP 94 total bilirubin 0.9, total globulin 2.90.9, total globulin 2.9

Hep A,B,C negative, negative PPDHep A,B,C negative, negative PPD

TSH 2.3TSH 2.3

Ferritin 276 PSA 0.3 Ferritin 276 PSA 0.3

Page 11: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

LabsLabs Stool studies grew out dientamoeba fragilisStool studies grew out dientamoeba fragilis Ultasound of abdomen—ascitesUltasound of abdomen—ascites

Paracentesis of ascitic fluid demostrated a high Paracentesis of ascitic fluid demostrated a high SAAG of 2.2 (Serum Albumin-4.2 Ascites Albumin SAAG of 2.2 (Serum Albumin-4.2 Ascites Albumin 2.0)2.0)

Spontaneous bacterial peritonitis diagnosed with Spontaneous bacterial peritonitis diagnosed with wbcs of 2,125 97% polyswbcs of 2,125 97% polys

Ascites cytology was negativeAscites cytology was negative

EGD, Colonscopy was plannedEGD, Colonscopy was planned

Page 12: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Differential DxDifferential Dx SAAGSAAG

Serum-to-ascites albumin gradient: Runyon et al (1992)

>=1.1g/dLCirrhosisAlcoholic Hepatitis CHFMassive hepatic metastasesVascular occlusionFatty liver disease of pregnancyMyxedema

<1.1 g/dlPeritoneal carcinomatosisNephrotic syndromePeritoneal TBPancreatitisBowel obst/per/infarctserositis

Page 13: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

EchocardiographyEchocardiography

Normal ejection fractionNormal ejection fraction

Mild to moderate MRMild to moderate MR

LA upper limits of normalLA upper limits of normal

No pericardial effusionNo pericardial effusion

Page 14: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

CT of chest and abdomenCT of chest and abdomen

Ascites, prominent liver and spleenAscites, prominent liver and spleen

No signs of cirrhosis or liver massNo signs of cirrhosis or liver mass

Chest CT revealed pericardial calcificationChest CT revealed pericardial calcification

Page 15: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC
Page 16: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC
Page 17: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Pericardial calcification

Page 18: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Right Heart CatheterizationRight Heart Catheterization Cardiac output 5.0 liters/minCardiac output 5.0 liters/min

RA 24/23 mmHgRA 24/23 mmHg

RV 40/25 mmHgRV 40/25 mmHg

PA 42/27 mm HgPA 42/27 mm Hg

PCW 27/25 mmHgPCW 27/25 mmHg

LV/LVEDP 100/23 mmHgLV/LVEDP 100/23 mmHg

Page 19: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

LV/RV simultaneous tracing reveals equilibrium of diastolic pressures

Page 20: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Dip and plateau configuration of the ventricular waveforms

Page 21: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

One month later….One month later….

Page 22: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC
Page 23: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC
Page 24: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC
Page 25: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC
Page 26: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Surgical pathology of pericardiumSurgical pathology of pericardium

Dense fibrosis and scattered chronic Dense fibrosis and scattered chronic inflammationinflammation

Page 27: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Constrictive PericarditisConstrictive Pericarditis

Heavily fibrosed or calcified pericardium restricts Heavily fibrosed or calcified pericardium restricts diastolic filling and results in elevation and diastolic filling and results in elevation and equilibrium of diastolic pressures of all four equilibrium of diastolic pressures of all four chambers of the heartchambers of the heart

Usually begins with initial episode of acute Usually begins with initial episode of acute pericarditis which may not be detectable clinicallypericarditis which may not be detectable clinically

Page 28: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Initial fibrin deposition often with pericardial Initial fibrin deposition often with pericardial effusioneffusion

Slowly progresses to a subacute stageSlowly progresses to a subacute stage

Organization and resorption of effusionOrganization and resorption of effusion

Chronic stage of fibrous scarring and thickeningChronic stage of fibrous scarring and thickening

Obliteration of pericardial space-majority of cases Obliteration of pericardial space-majority of cases visceral and parietal layers fusevisceral and parietal layers fuse

Page 29: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Disease progressionDisease progression Increase in systemic venous pressure-initially Increase in systemic venous pressure-initially

maintains diastolic filling of the ventriclesmaintains diastolic filling of the ventricles

Ultimately results in renal retention of sodium and Ultimately results in renal retention of sodium and water further increasing systemic venous pressurewater further increasing systemic venous pressure

Pericardial scar may reduce diastolic ventricular Pericardial scar may reduce diastolic ventricular volumesvolumes

Compensatory tachycardiaCompensatory tachycardia

Page 30: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Reduced cardiac output, tachycardia and elevated Reduced cardiac output, tachycardia and elevated right heart pressures may simulate myocardial failureright heart pressures may simulate myocardial failure

Systolic contraction of the ventricles and intrinsic Systolic contraction of the ventricles and intrinsic contractile state of the myocardium are usually contractile state of the myocardium are usually normalnormal

Severe cases-myocardial function may be depressed Severe cases-myocardial function may be depressed secondary to myocardial atrophy, fibrosis or secondary to myocardial atrophy, fibrosis or obliteration of the epicardial coronary arteries in the obliteration of the epicardial coronary arteries in the fibrotic scar causing ischemiafibrotic scar causing ischemia

Page 31: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

DiagnosisDiagnosis Symptoms of systemic venous congestionSymptoms of systemic venous congestion

Edema, abdominal swelling, ascites, passive Edema, abdominal swelling, ascites, passive hepatic congestionhepatic congestion

Postprandial fullness, dyspepsia, anorexiaPostprandial fullness, dyspepsia, anorexia

If right and left heart pressures elevatedIf right and left heart pressures elevated Orthopnea, dyspnea, coughOrthopnea, dyspnea, cough

Other symptoms-fatigue,weight loss, muscle Other symptoms-fatigue,weight loss, muscle wastingwasting

Page 32: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Physical findingsPhysical findings Elevated JVDElevated JVD

Kussmaul’s sign-inspiratory increase in systemic Kussmaul’s sign-inspiratory increase in systemic venous pressurevenous pressure

Pulsus paradoxus is uncommon in rigid constrictive Pulsus paradoxus is uncommon in rigid constrictive pericarditis unless pericardial effusion is presentpericarditis unless pericardial effusion is present

Diastolic pericardial “knock”-early diastolic sound Diastolic pericardial “knock”-early diastolic sound often heard along the left sternal borderoften heard along the left sternal border

Page 33: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

The knock represents sudden cessation of The knock represents sudden cessation of ventricular filling –higher frequency than S3 ventricular filling –higher frequency than S3 and may be confused with opening snap sound and may be confused with opening snap sound of mitral stenosisof mitral stenosis

Page 34: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Diagnostic toolsDiagnostic tools CXR-cardiac silhouette may be small, normal or enlargedCXR-cardiac silhouette may be small, normal or enlarged

Pericardial effusion-enlarged bordersPericardial effusion-enlarged borders

Calcification-helpful but does not equal percardial constrictionCalcification-helpful but does not equal percardial constriction

CT/MR-can identify pericardial thickening, dilation of vena CT/MR-can identify pericardial thickening, dilation of vena cavae and RV deformationcavae and RV deformation

***Significant pericardial constriction may occur in presence ***Significant pericardial constriction may occur in presence of diseased but minally thickened pericardiumof diseased but minally thickened pericardium

EKG –low voltage, afib, flutter, generalized T wave changes, EKG –low voltage, afib, flutter, generalized T wave changes, conduction defects…lots of stuffconduction defects…lots of stuff

Page 35: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC
Page 36: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

echocardiographyechocardiography Pericardial thickeningPericardial thickening

Effusions/calcificationsEffusions/calcifications

““septal bounce” –abrupt displacement of of interventricular septal bounce” –abrupt displacement of of interventricular septum during early diastolic fillingseptum during early diastolic filling

Hepatic/IVC dilationHepatic/IVC dilation

Inspiratory decrease in diastolic mitral inflow and increased Inspiratory decrease in diastolic mitral inflow and increased early diastolic tricuspid inflow(opposite changes occur with early diastolic tricuspid inflow(opposite changes occur with expiration)expiration)

Respiratory variation in doppler flow patterns may also Respiratory variation in doppler flow patterns may also suggest constriction vs restriction. suggest constriction vs restriction.

Page 37: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Cardiac CatheterizationCardiac Catheterization Elevation and equalization of diastolic filling Elevation and equalization of diastolic filling

pressurespressures

Catheterization of both ventricles should be Catheterization of both ventricles should be performed-elevation and virtual identical performed-elevation and virtual identical (within 5mmHg) right atrial, right (within 5mmHg) right atrial, right ventricular,left atrial, and left ventricular ventricular,left atrial, and left ventricular diastolic pressuresdiastolic pressures

Right and left ventricular diastolic pressures Right and left ventricular diastolic pressures show characteristic early diastolic dip show characteristic early diastolic dip followed by a plateaufollowed by a plateau

Page 38: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

.

Pressures in the left (LV) and right ventricle (RV) of a patient with constrictive pericarditis. During peak inspiration (arrow), there is a decrease in LV pressure and a concomitant increase in RV pressure, indicating discordance of ventricular pressures

Page 39: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Right atrial pressure characterized by Right atrial pressure characterized by preserved systolic x descent, a prominent early preserved systolic x descent, a prominent early y descent . A and V waves are small and equal y descent . A and V waves are small and equal in height –M or W configurationin height –M or W configuration

Page 40: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Varieties of constrictive pericarditisVarieties of constrictive pericarditis

Typical forms -Typical forms -chronic (calcific, rigid shell) -subacute (non-calcific, chronic (calcific, rigid shell) -subacute (non-calcific,

elastic)elastic)   

Effusive-constrictive  Effusive-constrictive 

LocalisedLocalised

congenitalcongenital

Page 41: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Etiologies of constrictive pericarditisEtiologies of constrictive pericarditis

TBTB Post-surgicalPost-surgical Prior mediastinal radiationPrior mediastinal radiation Connective tissue disorders-RA, SLEConnective tissue disorders-RA, SLE Drug-induced-procainamide,hydralazine,methysergideDrug-induced-procainamide,hydralazine,methysergide NeoplasticNeoplastic Trauma-induced inflammationTrauma-induced inflammation Infectious-bacterial, fungal, parasitic,viralInfectious-bacterial, fungal, parasitic,viral Post MI, post-pericardiotomy syndromePost MI, post-pericardiotomy syndrome IdiopathicIdiopathic congenitalcongenital

Page 42: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Treatment and prognosisTreatment and prognosis Diet and diureticsDiet and diuretics

Avoid calcium and beta blockers because mild sinus Avoid calcium and beta blockers because mild sinus tachycardia is a compensatory mechanismtachycardia is a compensatory mechanism

Complete resection of pericardium especially at diaphragmatic Complete resection of pericardium especially at diaphragmatic ventricular contactsventricular contacts

May have excessive bleeding, technically complex. High May have excessive bleeding, technically complex. High incidence of arrythmiasincidence of arrythmias

Mortality rates 5-15%Mortality rates 5-15%

Most patients achieve NYHA class 1 or 2 after surgeryMost patients achieve NYHA class 1 or 2 after surgery

Results are better with less calcium and when performed Results are better with less calcium and when performed earlier in disease courseearlier in disease course

Page 43: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

The end!!The end!!

Page 44: Wednesday Morning Conference December 14 th 2005 Kenneth Saland M.D. FACC

Constrictive vs RestrictiveConstrictive vs Restrictive     History -active pericarditis  History -active pericarditis  ECG absence of intraventricular conduction ECG absence of intraventricular conduction

defect defect  Chest radiograph pericardial calcification  Chest radiograph pericardial calcification  CT/MRI thickened pericardium  CT/MRI thickened pericardium  Echocardiogram septal notch  Echocardiogram septal notch  Doppler ventricular interdependence  Doppler ventricular interdependence  Cardiac catheterization close equilibration of Cardiac catheterization close equilibration of

diastolic pressures  diastolic pressures  Biopsy absence of amyloid or other infiltrative Biopsy absence of amyloid or other infiltrative

diseasedisease