Pericarditis and Cardiomyopathy Flashcards
Class 1 recommendations for pericardial disease echo
pts with suspected pericardial disease including effusion, constriction
pations with suspected bleeding in pericardium
follow up for recurrence
pericardial friction rub in MI with symptoms like pain nausea and hypotension
Thickened pericardium measurement
greater than 4mm
Pericardial anatomy
normally contains 5-30mL serous fluid
reflections create oblique and transverse sinus
fused with diaphragm
congenital absence of pericardium
mulibrey nanism
leads to CHF, constrictive pericarditis
normal spontaneous respirophasic variation
transtricuspid inflow increase by 20% on inspiration and decrease by 20% on expiration
transmitral inflow increase by 10% on expiration and decrease by 10% on inspiration
intrathoracic pressure from -3 to -6 with normal respirations
gradient for filling RV is RAP - negative intrathoracic pressure. Increased RV filling, decreased LV filling during inspiration
increased LV filling , decreased RV filling during expiration
Septum shifts to left
negative pressure inspiration
less rv afterlaod
increased rv filling
decreased lv filling
increased lv afterload
negative pressure expiration
decreased systemic venous return
decreased rv filling
increased rv afterload
increased LV filling
decreased LV afterload
CP and tamponade with spontaneous variation
changes of inspiration and expiration exaggerated in both with spontaneous ventilation
Tamponade changes with ppv
decrease in variation. So much that you can end up causing arrest
Constrictive pericarditis
increased resp variation with both spont and ppv
elevated and equalized CVP , Pulm vein and LVEDP
prominent early filling (exagerrated Y descent)
pulus paradoxus uncommon but kussmauls sign common
tamponade
increased resp variation with spontaneous
decreased resp variation with ppv
elevated and equalized cvp, pulm vein and LVEDP pressures
prominent systolic filling (loss of y descent)
pulsus paradoxus common
kussmauls sign uncommon
congenital pericardial problems
rare
partial or total absence
mulibery nanism (muscle liver brain eye nanism) = chf and CP
pericarditis
inflammation of pericardium
Triad : chest pain, ekg changes (diffuse st elevation) , friction rub at left sternal border with pt leaning forward. Pain better leaning forward
Chronic can lead to constrictive
Often idiopathic / viral
infection
neoplastic
autoimmune
post surgical
post radiation
drugs/ trauma/ uremia
thickness usually greater than 4mm but not always. Use MRI>CT=TEE>TTE
CP vs RICM
peak velocity pulm vein D wave variation > 18%
peak velocity TM E wave variation >10% in CP
color m mode Vp >100cm/sec in CP
Tissue doppler e’<8 cm/sec in RICM
Tissue doppler septal velocity > lateral velocity in CP
pericardial knock in cp, s3 in RICM
BNP <100 pg/ml in CP but elevated in RICM
thickness >4mm favors CP
tissue doppler cp vs ricm
e’<8cm/sec in ricm
e’>10 cm/sec in cp
annulus reversus lat e’<sep e’ in CP
annulus paradoxus E/e’ <15 in CP
hepatic venous reversal spontaneous
cp- reversal during expiration
ricm- reversal during inspiration
pulm venous resp variation spontaneous
peak velocity d wave variation >18% in cp
MRI comparison of cp vs ricm
late gad enhancement of pericardium and thick - cp
lge of sub endocardium - ricm
LA : RA volume CP»RICM
Max septal excurtion b/w in and ex cp>RICM
speckle tracking differences
cp- ratio of LV free wall strain to septal wall strain and RV were less in CP than RICM
Vp
<50 cm/sec = ricm
>100 cm/sec=cp
cardiac cath cp vs ricm
elevation and equalization of diastolic pressures in cp
lvedp>rvedp in ricm
dip and plateau sign
square root sign seen in both cp and ricm that indicates rapid early filling
tamponade findings
tachycardia
chest pain/fullness
dyspnea, tachypnea
peripheral edema
hypotension
Elevated JvP without kussmaul
pulsus paradoxus but may be absent if regional/loculated
chamber collapse for tamponade
absence = very unlikely there is tamponade
RA collapse >1/3 cycle is nearly 100% sens and specific
RV collapse occurs iin diastole
RA collapse in diastole can be normal
pericardial effusion
0.5 and less is small
.5-2 cm moderate (200-500 mL)
>2cm large
tamponade doppler changes
prolongation IVRT
decrease or reversal of hepatic d waves w expiration
when is pulsus paradoxus seen besides tamponade
copd, asthma, vigorous positive pressure ventilation
mitral inflow patterns for tamponade and constrictive pericarditis
tamponade - impaired relaxation with a >e
cp - restrictive pattern with e»a
pericardial tumors
not high yield
primary: benign more comon. teratoma, lipoma, fibroma ,hemangioma, lymphangioma
malignant-mesothelioma, angiosarcoma
Secondary: metastatic, more common than primary. Lymphoma, melanoma, lung ,breast carcinoma. usually present with pericardial effusion
pericardial cysts
congenital or infectious
enclosed spaces taht do not communicate with pericardial space. manage conservatively
How much fluid is normal in pericardium?
25-50 mL
Does VSD typically cause RV or LV enlargement
usually LV , especially at first. All flow goes from LV to RV and out pulmonic valve during systole
what is pulsus alternans
alternating strong and weak beats seen on arterial line. Associated with severe LV systolic dysfunction
what is kussmaul sign
paradoxical rise in RAP during inspiration. Commonly seen in constrictive pericarditis and RICM as there is a decrease in RV compliance.
E/e’ ratio for CP
usually less than 15
Annulus paradoxus
LVDP in CP
unchanged. LV is shielded from decrease in pressure due to constrictive pericarditis.
There is an exaggerated decrease in LV filling
3 major types of cardiomyopathy
Dilated- not enough stuff. 100% have systolic dysfunction. Carpentier 3B. Most common cardiomyopathy
Hypertrophic-Too much stuff. AD variable penetrance and expresivity. LVOT obstruction 25% pts. 100% have diastolic dysfunction. Have subendocardial ischemia and vtach. Get pacemakers that cause RBBB to reduce obstruction. Associated with cardiac death sudden
RICM- the wrong stuff. Amyloidosis most common. 100% have diastolic dysfunction. Prognosis related to thickness of walls and diastolic dysfunciton. Systolic function also eventually gets worse.
ONce symptoms appear 2-3 year survival is less than 50%
Dilated cardiomyopathy
causes 3b carpentier mitral motion.
Caused by: idopathic, peripartum, infectious, toxin, genetics.
Associated with low EF, low flow leading to LAA clot / LV clot
Toxic causes of dilated cardiomyopathy
cobalt, doxorubicin, alcohol, snake bites
infectious causes of dilated cardiomyopathy
chagas, post viral
Children can get severe acute form after virus that can improve and return to basically normal
Higher mortality in D CM
EDD of >4cm/m2
HOCM / HCM
Obstuction occurs in 25%. AD with variable penetrance and expressivity
4 types based on pattern of hypertrophy. Basal inferolateral wall is spared in all
usually normal systolic function but 100% have diastolic dysfunction
Reguritant jet is posteriorly directed (y sign)
CWD of HOCM
Late systolic peaking , dagger shaped
M mode of HOCM aortic valve
Early systolic closure and fluttering
RICM
Infiltration of myocardium from abnormal substances. Leading to stiff myocardium.
Primary; loefflers hypereosinophillic, endomyocardial fibrosis, idiopathic
Secondary: amyloid, sarcoid, glycogen storage disease, hemochromotosis, Drugs, radiation
Echo appearance of RICM
granular speckled , starry sky appearance of myocardium
Transmitral inflow velocities in ricm
restrictive pattern like CP but also has reduced tissue doppler
4 types of HCM
sigmoidal (most common basal septal )
reverse curve - entire septum
apical
neutral-concentric
other findings often seen in addition to enlarged septum in HCM
elongated leaflet and apically displaced papillary muscle
Different gradients seen in HCM
LVOT (web, SAM)
Mid Cavitary
Diastolic apical gradient
Gradient of LVOT at rest that pt need to go on for surgical consult
greater than 50
LVOT gradient with exercise or provocation (dobutamine) indicating SAM/MR
greater than 30
