Constrictive pericarditis

1. CONSTRICTIVECONSTRICTIVE
PERICARDITISPERICARDITIS
MAJ WAQAS KHALIDMAJ WAQAS KHALID

2. •CONSTRICTIVE PERICARDITISCONSTRICTIVE PERICARDITIS —result of scarring and—result of scarring and
consequent loss of elasticity of the pericardial sac.consequent loss of elasticity of the pericardial sac.
Typically chronic. The pathological changes areTypically chronic. The pathological changes are
inflammation, sometimes calcification. Grossly,inflammation, sometimes calcification. Grossly,
pericardium thicker than normal -80% of time.pericardium thicker than normal -80% of time.
•EFFUSIVE-CONSTRICTIVE PERICARDITISEFFUSIVE-CONSTRICTIVE PERICARDITIS ——
characterized by constrictive physiology with acharacterized by constrictive physiology with a
coexisting pericardial effusion, usually with tamponade.coexisting pericardial effusion, usually with tamponade.

3. PERICARDIUMPERICARDIUM
Upto 50 mL fluid
Parietal and visceral layers

4. ANATOMYANATOMY
• Lt. AtriumLt. Atrium is notis not
completelycompletely
intrapericardialintrapericardial
• All other cardiacAll other cardiac
chamberschambers areare
completelycompletely
intrapericardialintrapericardial
• Pulmonary Veins arePulmonary Veins are
completelycompletely
intrathoracic (extraintrathoracic (extra
pericardial)pericardial)

5. PHYSIOLOGY OF CONSTRICTIONPHYSIOLOGY OF CONSTRICTION
• In the pericardial compressive syndromes, theIn the pericardial compressive syndromes, the
pericardium is inelastic andpericardium is inelastic and total cardiac volumetotal cardiac volume
cannot changecannot change
• The result is enhanced ventricular interaction or…The result is enhanced ventricular interaction or…
ventricular interdependenceventricular interdependence

6. PHYSIOLOGY OF CONSTRICTIONPHYSIOLOGY OF CONSTRICTION
• Pericardial constriction leads to impairment ofPericardial constriction leads to impairment of
ventricular filling, usually affecting all four cardiacventricular filling, usually affecting all four cardiac
chambers, preventing ventricular filling in mid andchambers, preventing ventricular filling in mid and
late diastole.late diastole.
• As a result, the majority of ventricular filling occursAs a result, the majority of ventricular filling occurs
rapidly in early diastole and the ventricular volumerapidly in early diastole and the ventricular volume
does not increase after the end of the early fillingdoes not increase after the end of the early filling
period.period.

7. EFFECT OF INSPIRATIONEFFECT OF INSPIRATION
• Normal PericardiumNormal Pericardium::
• Inspiratory decrease in intrathoracic pressure isInspiratory decrease in intrathoracic pressure is
uniformly transmitted to the lungs, PVs, and alluniformly transmitted to the lungs, PVs, and all
cardiac chamberscardiac chambers..
• Decrease in PCWP accompanied byDecrease in PCWP accompanied by
corresponding decrease in LV Pressurecorresponding decrease in LV Pressure
• Normal pericardium contributes to diastolicNormal pericardium contributes to diastolic
interaction ( transmission of intracavitary fillinginteraction ( transmission of intracavitary filling
pressures to adjoining chambers)pressures to adjoining chambers)

8. EFFECT OF INSPIRATIONEFFECT OF INSPIRATION
Constrictive PericarditisConstrictive Pericarditis::
•Pulmonary veins and LA extra pericardial structures.Pulmonary veins and LA extra pericardial structures.
•Thickened pericardium isolates the heart formThickened pericardium isolates the heart form
transmission of intrathoracic pressure changestransmission of intrathoracic pressure changes
•Inspiratory decrease in intrathoracic pressureInspiratory decrease in intrathoracic pressure
transmitted to pul veins and LA but not to LVtransmitted to pul veins and LA but not to LV
•Decrease in PCWP not accompanied by correspondingDecrease in PCWP not accompanied by corresponding
decrease in LV pressure causing less gradient anddecrease in LV pressure causing less gradient and
decreased LV fillingdecreased LV filling
•Allows increased RV filling and IVS shift to left.Allows increased RV filling and IVS shift to left.

10. CONSTRICTIVECONSTRICTIVE
PERICARDITIS - ETIOLOGYPERICARDITIS - ETIOLOGY
• Idiopathic or viral — 42 to 49 %Idiopathic or viral — 42 to 49 %
• Post cardiac surgery — 11 to 37 %Post cardiac surgery — 11 to 37 %
• Post radiation therapy — 9 to 31 %Post radiation therapy — 9 to 31 %
• Connective tissue disorder — 3 to 7 %Connective tissue disorder — 3 to 7 %
• Post infectious (Post infectious (tuberculoustuberculous or purulent pericarditis)or purulent pericarditis)
— 3 to 6 % (— 3 to 6 % ( Most common in our setup)Most common in our setup)
• Miscellaneous causes (malignancy, trauma, drug-Miscellaneous causes (malignancy, trauma, drug-
induced, asbestosis, sarcoidosis, uremicinduced, asbestosis, sarcoidosis, uremic
pericarditis) — 1 to 10 %pericarditis) — 1 to 10 %

11. CONSTRICTIVE PERICARDITIS –CONSTRICTIVE PERICARDITIS –
CLINICAL PRESENTATIONCLINICAL PRESENTATION
• 67 % presented with symptoms of Right heart failure (HF)67 % presented with symptoms of Right heart failure (HF)
• 8 % with chest pain8 % with chest pain
• 6 % with abdominal symptoms6 % with abdominal symptoms
• 4 % with atrial arrhythmia4 % with atrial arrhythmia
• 5 % with symptoms of cardiac tamponade5 % with symptoms of cardiac tamponade
• Constrictive pericarditis can be mistaken for any cause ofConstrictive pericarditis can be mistaken for any cause of
right heart failure as well as end stage liver diseaseright heart failure as well as end stage liver disease

12. • Most patients have thickened pericardiumMost patients have thickened pericardium
• Normal thickness on direct histopathologicalNormal thickness on direct histopathological
examination (18%) and on CT scanning ( 28%)examination (18%) and on CT scanning ( 28%)
• Transient constrictive pericarditis ( Post cardiacTransient constrictive pericarditis ( Post cardiac
surgery)surgery)
CONSTRICTIVE PERICARDITISCONSTRICTIVE PERICARDITIS

14. CONSTRICITVE PERICARDITIS –CONSTRICITVE PERICARDITIS –
PHYSICAL EXAMINATIONPHYSICAL EXAMINATION
• Elevated JVP with prominent Y descentElevated JVP with prominent Y descent
• Peripheral edemaPeripheral edema
• AscitesAscites
• HepatomegalyHepatomegaly
• Pleural effusionPleural effusion
• Pericardial knockPericardial knock
• Pulsus paradoxus ( 1/3 rd of patients only)Pulsus paradoxus ( 1/3 rd of patients only)
• Kussmaul’s signKussmaul’s sign
• Cachexia- late stagesCachexia- late stages

15. • Inspiratory increase in mean venous pressureInspiratory increase in mean venous pressure
or the pressure may simply fail to decrease onor the pressure may simply fail to decrease on
inspirationinspiration
• Reflects loss of normal increase in right heartReflects loss of normal increase in right heart
venous return on inspiration, even thoughvenous return on inspiration, even though
tricuspid flow increasestricuspid flow increases
• Absent in tamponadeAbsent in tamponade
Kussmaul’s sign

16. KUSSMAUL’S SIGNKUSSMAUL’S SIGN

17. PERICARDIAL THICKENINGPERICARDIAL THICKENING
• This can be visualized by transesophageal echoThis can be visualized by transesophageal echo
(often requiring multiple views), however, this is(often requiring multiple views), however, this is
best seen using other imaging modalities such asbest seen using other imaging modalities such as
CT or MRI.CT or MRI.

18. CALCIFIED PERICARDIUMCALCIFIED PERICARDIUM

19. PERICARDIAL CALCIFICATIONSPERICARDIAL CALCIFICATIONS
CTCT

20. PERICARDIAL CALCIFICATIONPERICARDIAL CALCIFICATION
ON ECHOON ECHO
• Normal pericardium is highlyNormal pericardium is highly
reflectivereflective
• Bright pericardial echoBright pericardial echo
cannot alone diagnosecannot alone diagnose
constrictive pericarditisconstrictive pericarditis

21. SPECIFIC ECHO EXAM FORSPECIFIC ECHO EXAM FOR
CONSTRICTIONCONSTRICTION
• Neither sensitive nor specificNeither sensitive nor specific
• Must diagnose via a combination of physicalMust diagnose via a combination of physical
exam/ history findings and echo findingsexam/ history findings and echo findings

22. M-MODE FINDINGS INM-MODE FINDINGS IN
CONSTRICTIONCONSTRICTION

23. DILATION AND LACK OFDILATION AND LACK OF
RESPIRATORY VARIATION IN IVCRESPIRATORY VARIATION IN IVC

24. DIASTOLIC SEPTAL BOUNCE:DIASTOLIC SEPTAL BOUNCE:
• Thought to be due to the rapid filling during earlyThought to be due to the rapid filling during early
diastole leading to asymmetrical filling of the rightdiastole leading to asymmetrical filling of the right
and left ventricals which creates a fluctuatingand left ventricals which creates a fluctuating
pressure gradient that manifests as an abrupt shift ofpressure gradient that manifests as an abrupt shift of
the septum.the septum.

26. SEPTAL BOUNCE ON ECHO ANDSEPTAL BOUNCE ON ECHO AND
MRIMRI

27. ATRIAL DILATIONATRIAL DILATION
• MildMild
• Secondary to elevated atrial pressuresSecondary to elevated atrial pressures
• More severe atrial dilatation seen inMore severe atrial dilatation seen in
restrictive cardiomyopathy.restrictive cardiomyopathy.

30. DOPPLER ECHO FINDINGS INDOPPLER ECHO FINDINGS IN
CONSTRICTIONCONSTRICTION

33. UN MASKING RESP VARIATIONSUN MASKING RESP VARIATIONS

35. TISSUE DOPPLER TOTISSUE DOPPLER TO
DISTINGUISH ENTITIESDISTINGUISH ENTITIES
Dimunitive E’
<8 cm/s
E’ similar to E
>12cm/s

38. DOPPLER ECHO AND RESPDOPPLER ECHO AND RESP
VARIATIONSVARIATIONS

44. VENTRICULARVENTRICULAR
INTERDEPENDENCEINTERDEPENDENCE
Insp Expir
Hatle LK, et. al.
Circ. 1989;79357-370
Ventricular Pressures
Are DISCORDANT

45. CONSTRICTIVE PERICARDITIS –CONSTRICTIVE PERICARDITIS –
OTHER TESTS?OTHER TESTS?
• ECG sync CT – helps in detecting minute amount ofECG sync CT – helps in detecting minute amount of
calcification. Important adjunt to Doppler echocalcification. Important adjunt to Doppler echo
examinationexamination
• Cardiac MRI – Role in diagnosing transient post opCardiac MRI – Role in diagnosing transient post op
constrictive pericarditis( late gadolinium enhancementconstrictive pericarditis( late gadolinium enhancement
and pericardial thickness > 3mm)and pericardial thickness > 3mm)
• BNP – usually only a mild elevation due to limited wallBNP – usually only a mild elevation due to limited wall
stretchstretch

46. EFFUSIVE CONSTRICTIVEEFFUSIVE CONSTRICTIVE
PERICARDITISPERICARDITIS
• Combination of tamponade and constrictionCombination of tamponade and constriction
• Common etiologies: malignancy and radiation therapyCommon etiologies: malignancy and radiation therapy
• Pericardial thickening may prevent RA collapsePericardial thickening may prevent RA collapse
• Hemodynamic compromise and JVD persist even after tapHemodynamic compromise and JVD persist even after tap

47. TREATMENTTREATMENT
• Surgical pericardiectomy is definitive treatment except transientSurgical pericardiectomy is definitive treatment except transient
constrictive pericarditisconstrictive pericarditis
• Patients with major comorbidities or severe debilitation and radiationPatients with major comorbidities or severe debilitation and radiation
induced disease are relatively contraindicated for pericardiectomyinduced disease are relatively contraindicated for pericardiectomy
• Medical management with diuretics and salt restrictionMedical management with diuretics and salt restriction
• Because sinus tachycardia is a compensatory mechanism beta blockersBecause sinus tachycardia is a compensatory mechanism beta blockers
and Ca antagonists should be avoidedand Ca antagonists should be avoided
• In pattients with AF and rapid vent response, digoxin is recommendedIn pattients with AF and rapid vent response, digoxin is recommended
• Patients with late gadolinium enhancement on MRI and pericardialPatients with late gadolinium enhancement on MRI and pericardial
thickness of more than 3 mm should be considered for a trial of antithickness of more than 3 mm should be considered for a trial of anti
inflammatory therapy for 2-3 months.inflammatory therapy for 2-3 months.

50. ThanksThanks
ForFor
Listening!!Listening!!