Cardiac Flashcards
what is the RA defined by?
IVC
what imp structures are in the RA?
- crista terminalis
- Eustachian valve
eustachian valve
-valve of IVC
chiari network
Eustachian valve (IVC) trabeculated appearance
coronary sinus route
AV groove –> RA
what defined right Vt?
moderator band
TV vs MV
TV papillary m inserts on septum. No fibrous conn btw TV and P
signs of LA enlargement
double density (direct) splaying carina (indir) walking man sign (indir)
walking man sign
pst displacement left main stem bronchus on lateral radiograph –> upside down V w/ intersection of right bronchus
MV
-papillary m inserts on lateral/pst walls and apex left Vt (not septum)
echogenic focus in LV
- calcified papillary m
- resolve by 3rd TM
- 13% ass w/ DS
lipomatous HTr interatrial septum
- dumbbell/bilobed, SPARES F.O.
- obese, elderly
- asyx (supraVt arryth)
- brown fat –> HOT on pet
multiple interatrial lipomas
TS
interatrial fatty lesions
- lipomatous HTr interatrial septum-dumbbell, spares f.o.
- lipoma- encapsulated, does not spare f.o
- both PET-HOT
interatrial lipoma
- encapsulated
- normal fat signal on MR
- pet hot
coronary cusps
R, L, non (pst)
right coronary branches
- conus (ant), 20-30% from aorta–> RVOT
- SA (pst)
- acute marginal–> RV free wall
- AVN-junction of av/iv
- PDA (65-80%)–> pst IV septum
- PLA–> pst LV
how often does RCA perfuse SA and AV node?
SA-60%
AV-90%
dominance
R (85%)-PDA, PLA from RCA
L (7%)-PDA, PLA, AVN from left CX
co (7%)-PDA from RCA, PLA from left CX
order of obtaining chamber views
- axial –> 2 chamber/vertical long axis –> 4 chamber view/horz long axis. –> short axis
- 3 chamber/LVOF/apical long axis view
dividing anomalies of coronary arteries
org, course, termination
benign anomalies of coronary artery
does not course btw aorta and pulmonary a
-retroaortic, prepulmonic, septal
anomalies of coronary arteries that are always malignany
arise from pulmonary artery
-ALCAPA (bland-white-garland syndrome) > ARCAPA
potentially malignant anomalies of coronary arteries
- LCA from RCS
- RCA from LCS
- LCx or LAD from RCS
- a from NCS
LCA branches
- btw PA and LAA
- LAD, Lcx, ramus (15%)
- LAD–> ant IV septum. Diagonal –> anterolat wall. Septal –> septum
- Lcx –> AV groove. OMA –> pstlat LV
bland white garland syndrome
ALCAPA
compl malignant anomalous courses of CAs. Rx.
- sudden cardiac death w/ exercise
- Rx= surgical bypass
Mx ALCAPA/ARCAPA
- children: direct implantation of anomalous CA
- adults: bypass
pres ALCAPA/ARCAPA
85% CHF ~2 mo old
intramural course of coronary artery-app, compl, mx
- short segm course through aortic wall (slit-like)
- SCD
- mx=
- intramural coronary a bypass, reimplantation
- unfooring
myocardial bridging-MC location, syx, mx,
- midLAD
- asyx; angina, MI, dead-(+) during systole and w/ depth
- dx-stress test
- mx-BB, CCB, PCI, sx (unroofing, myotomy, CABG)
MC (and most serious) malignant org
-interarterial LCA from RCS
mx interarterial LCA from RCS and RCA from LCS
- left: repair
- right: repair if syx
mcc’s SCD
1) hypertrophic cardiomyopathy
2) interarterial LCA from RCS
types ALCAPA
1) infantile
2) adult
coronary artery steal syndrome
ALCAPA
-reversed flow in LCA as P decrease in pulmonary circulation
ALL OF THE CA ANOMALIES to consider
- benign-retroaortic, prepulmonic, septal
- interarterial LCA from RCS
- IA RCA from LEC
- ALCAPA
- ARCAPA
- intramural course
- myocardial bridging
CA aneurysm-size, causes
- 5x
- MC-ather, Kawasaki in kids, cath
coronary fistula
- btw CA and cardiac chamber or GV
- RCA –> r heart –> big, dilated CAs (coronary aneurysms)
main people who get coronary CT
1) low risk, atypical
2) anomalies
mx given prior to coronary CT
- bb (HR <60)
- NG
BB CI
- asthma, COPD, 2nd/3rd˚ HB, acute cp, recent cocaine use
* use retrospective gating
NG CI
- hypoTN (<100)
- severe AS
- HOCM
- phosphodiesterase (viagra, sildenafil)
how to quantify velocity of flowing blood
velocity-encoded cine MR/velocity mapping/phase-contrast
Ortner’s Syndrome
hoarseness caused by L recurr laryngeal n ISO LA enlargement
mc cong cardiac abN
- bicuspid (although pres in adulthood)
- VSD
3 types of bicuspid aortic valve
-sub, supra, valvular (90%)
supravalvular AS
williams syndrome
BC AV + CoArc
-turners syndrome
compl BC AV
- AS=mc
- cystic medial necr –> aortic aneurysm, AR
AR causes
- BC AV
- endocarditis
- marfans
- htn induced aortic root dilation
- aortic diss
rheumatic fever heart disease
- group A beta hemolytic strep
- acute-pancarditis
- chronic-inflamm valves –> fibrinoid necrosis in cusps & cords –> valvular/ct thickening, commisure fusion
- stenosis > mixed
- MV > AV (Rare to have isolated AV) > TV > PV
pulmonic stenosis divisions, causes
95% congenital (TOF), usually isolated
- supravalvular (williams)
- valvular-MC. –> Vt Htr. Noonans.
- subvalvular-Alagille syndrome (kids w/ ø bd’s)
AS causes
- htn
- BC AV
- williams syndrome (supravalvular)
BC AV ass
- Turners
- CoArc
- ADPKD
- VSD, PDA
mitral stenosis
-RF MCC
pulm regurg
failure TOF valve sx
-mx: okay if fixed before 150mL end-diastolic
TR
- pulm htn=mc
- endo
- carcinoid
testable pearl re: TR affect on RV
dilation, not Htr
Epstein anomaly-causes, app
- sporadic (mc), moms on Li
- TV hypoplasia, pst leaf displaced apically –> RA+, RV atrialized (-), TR
- “box shape” on cxr
left valvular carcinoid
1) 1˚ bronchial carcinoid
2) R to L shunt
Aortic Arch variants
2:
- bovine (common org left BCA and LCA)-MC branch variant
3:
- Right arch w/ mirror branching (cong heart) or left arch w/ mirror branching
- innominate brachiocephalic
- -pulmonary sling-left pulm artery arises from R
4:
- left arch aberrant right SCA-MC vessel anomaly
- R arch aberrant left SCA
- L vert off the aorta
- double aortic arch (R CCA SCA, L SCA CCA)-MC vascular ring
“mirror branching”
arch relationship to trachea
Right mirror branching vs right arch w/ aberrant subclavian
- mirror: subclavian arise from FRONT of arch
- subclavian-back of arch
vessels off double aortic arch
from R–> L: R CCA –> L SVA –> R SVA –> L CCA
R arch with mirror branching-ass
- asyx
- stronger ass w/ Truncus BUT TOF MC overall
- 90% w/ RAMB have TOF (6% truncus)
- pts with truncus- 33% MIRA, 25% TOF
what completes the ring in right arch L SVA
lig arteriosum around trachea
L arch aberrant R CVA
- dysphagia lusorum
- divertiulum kommerell
SS phenomenon vs syndrome
syndrome=cerebral ischemic symptoms
causes SS phenom/syndrome
atherosclerosis 98%
-Takayasu, radiation, preductal aortic coarctation, black-Taussig Shunt
heart tumors in kids
1) rhabdomyoma- MC. Hamartoma. TS. LV.
- those NOT ass w/ TS less likely to regress
- T2+
2) fibroma-2nd MC. IV septum.
- Dark. enh+++ (and delayed)
heart tumors adults
- mets- MC. pericardium.
- angiosarc-mc 1˚ mal. RA + pericardium
- big bulky, ugly
- “sunray”-enhancement along epicardial vess
- myxoma-mc 1˚ tumor. LA on interatrial septum, prolapse thru MV.
metastatic involvement of heart
pericardium (effusion, ln)
-Melanoma Myocardium
mc met to heart
lung
myxoma ass
MEN syndrome, Blue Nevi (Carney complex)
Aunt Minnie congenital heart appearances: egg on string, snow man, boot shaped, figure 3, box shaped, scimitar sword
- transposition
- TAPVR
- TOF
- CoA
- Ebstein
- PAPVR w/ hypoplasia
big box on cxr
-ebsteins
infantile hemangioendothelioma
vein of Galen malformation
6 T’s of cyanosis
TOF TAPVR Transposition Truncus TA
non-cyanotic
ASD VSD PDA PAPVR Aortic CoA (adult type-post ductal)
systematic approach to cong heart dx:
cyanotic or not (they must tell you)
R vs L arch
-R arch –> pulm vasc: (+) w/ truncus, (-) with TOF
- L arch–> Heart size
- massive (ebsteins or pulm atresia w/o VSD), non cardiac (infantile hemangioendothelioma, v of Galen malformation)
- Normal size: pulm blood flow
- (+) TAPVR, D transposition, Truncus, Single Vt
- (-) TOF, tricuspid atresia, Ebsteins
CHF in newborn
- TAPVR (infra cardiac type III)
- congenital AS or MS
- left sided hypoplastic heart
- cor triatritum
- infantile (pre-ductal) CoA
survival dep on admixture
- TAPVR (PFO)
- Transposition
- TOF (VSD)
- TA (VSD)
- hypoplastic Left heart-ASD (or large PFO) + PDA
small heart ddx
- adrenal insufficiency (Addisons)
- cachectic state
- constrictive pericarditis
VSD img
- big heart (splaying carina), inc vasc, small aortic knob
- membranous MC
- 70% small ones close spon’t
- outlet subtypes (infundibulum) must be repaired as R coronary cusp prolapses into defect
PDA
1) prematurity
2) maternal rubella
3) cyanotic heart disease
PDA closure
functionally 24 hr
anatomically 1 mo
PDA img
-big heart, big vasc, ductus bump
ASD sinus venosus association
PAPVR
types of asd
- primum, av canal, sinus venosum
- secundum-MC
which asd will not close via closure device?
- primum (too close to valve tissue)
- AV canal
cong heart dx most strongly ass w/ downs?
AV canal (primum)
unroofed coronary sinus
- 2 way flow
- paradoxical emboli and chronic R heart volume overload
PAPVR
1 of 4 veins draining into RA
-ASD (secundum, sinus venosum)
PAPVR + hypoplasia
scimitar
TAPVR
4 pulm v–> right heart
- big heart, big vasc (type III=newborn CHF)
- large PFO (required for survival.) ASD less common
- asplenia
TAPVR types
1) Supracardiac-MC. Snowman (S for S)
2) Cardiac-2nd MC
3) Infracardiac-v’s drain below diaphragm (hepatic or IVC)
why does type 3 TAPVR give newborn CHF?
veins draining to IVC/hepatic v’s obstructed on way through diaph
asplenia and cong heart disease stats
- 50% asplenia have cong heart dx.
- Of these, ~100% TAPVR and 85% additional endocardial cushion defects
Transposition of GV-what defines transposition, what defines D vs L type? Ass?
- transposition: AV ant to PV
- D vs L- AV to right vs L of PV
- VSD (mc), PDA (D-type), ASD
- D type-Vt/vess CONCORDANCE. PDA+ (nec to live)
- L type= DISCORDANCE: LA–> RV –> aorta (congenital correction), no PDA
- L type Lucky enough to Live
Ass: VSD (40%), supra or subvalv stenosis (30%)
D type transposition
- defined by aorta R of pulm A (like normal) but is ANT, not normal pst
- egg on a shell
- rx-inter-atrial baffle (mustard/senning procedure)
- classic draped look
MCC of cyanosis during first 24 hrs
transposition
MC cyanotic heart disease
tetralogy of fallot (TOF)
4 findings of tetralogy of fallot. What makes a pentralogy? Ass?
1) VSD
2) RVOT (due to infundibulum hypoplasia)
3) overriding aorta
4) RV Htr-determines severity
* pentralogy if ASD
* right arch very likely (1/4)
Rx TOF
- surgical
- Blalock-Taussig (shunt procedure)-if inoperable or bridge
- MC compl=PV regurg
truncus arteriosis-associations
- VSD, R arch
- CATCH-22 genetics (DiGeorge Syndrome)
CoA two types
infantile vs adult
CoA ass
- Turners syndrome (15-20%)
- Bicuspid AV (80%)
- berry aneurysms
- VSD
- PDA
CoA rib notching
-4th-8th ribs (not 1st & 2nd bc those fed by costocervical trunk)
hypoplastic left heart
LV, aorta
-need ASD or large PFO
+large PDA
-ass: aortic CoA, endocardial fibroelastosis
Cor Triatriatum Sinistrum
pulm v w/ fibromuscular mem –> LA –> subdivided LA (tri-atrium)
- acts like MS-pulm HTN, edema
- poor outcome
infantile vs adult CF
- infantile (preductal/SVA): R <3 fx, hypoplastic AArch
- adult (postductal/SVA): BP diffs, collaterals
normal am of fluid in pericardial space
50 cc
causes pericardial effusion
- renal fx (uremia)-mc
- lupus
- dressler
surgeries for hypoplastic left lung
- palliative, 3 step process (avoids R <3 overload)
1) Noorwood/Sano-day’s (N-newborn)
2) Glen-3-6 mo (G is 6th letter of alphabet)
3) Fontan-1.5-5 year (F=Five)
heart tx types
- orthotropic-who heart except part of atrium where pulm v’s attache
- heterotopic-adding donor to recipient heart (good for back up)
angiosarcoma
mc 1˚ mal.
RA (Really Angry) + pericardium
-big bulky, ugly
-“sunray”-enhancement along epicardial vess
Myxoma-who, where, img
- mc 1˚ cardiac tumor.
- 30-60 yo, distal emboli & fainting spells
- younger=syndromic (Carney complex)
- central LA on interatrial septum, from FO (trying to spread friendliness)
- Ca+ 25%, dystrophic, in areas of hemorrhage.
- mobile/prolapse thru MV.
- MR: T2+, var (but at least mild) enh. Variable sign based on tissue comp
- CT: intermediate density
fibroelastoma
- 2nd mc 1˚ cardiac tumor
- 50-60yo, asyx (or syx from emboli/stroke/tia)
- Aortic valve (on side of aortic cusp) (swinging from valves bc so elastic)
- small <1cm
- vs vegetations-veg involve valve free edge
mc intracardiac mass
thrombus
- LAA-A-fib
- LVt-MI
congenital/acquired absence pericardium
- partially over LA, adj PA –> shift towards L –> contact L cw
- tongue of lung btw aorta and PA
- risk of herniation & volvulus s/p extra pleural pneumonectomy. LAA most at risk.
cardiac mets
- lung (MC)/
- melanoma (only one that’s T2+)
- breast
(love me blood)
left sided central venous catheter
- L SVC, left intramammary vein, left superior intercostal vein, LUL partial anomalous vein
- arterial
- extravascular
etiology of L SVC
persistent pst cardinal v
purpose of pacemaker, ICDC (implantable cardioverter defibrillator), biVt ICD, epicardial pacer
- pacemaker-paces during bradycardia
- ICDC-defibrillates to prevent arrest; cardiomyopathy; decreased EF (his of Vt achy, fib, sad)
- biVt-syndronization in BBB
- epicardial pacer-post surgical pacing; removed after d’s
conduction devices
-pacemaker
-ICDC
-wireless (micra)
-subcut ICD (presternal lead att to side box; doesn’t pace)
-
purpose of loop recorders
-for palpations, syncope
types of valve repairs and diffs
- mechanica=20yrs, anticoag
- bioprosthetic-10-14 yrs, no anticoagulant
cardiac assist devices
- LVAD
- Impella
- IABP
closure devices
-ASD-amplatz, umbrella rashkind
LAA-amplatz, watchman
-pda-amplatz
scimitar-indicated in adults w/ pulmonary volume overload; R heart dilation
division of time frame post op CABG complications
- early= <1 mo
- late = >1 mo
grafts mC used in CABG
- saphenous v = #1
- internal mammary a=#2
- radial a, IMA,
arterial vs venous CABG grafts
Venous grafts have demonstrated a tendency to develop partial or complete occlusions with time, whereas arterial grafts have shown relative resis- tance to plaque formation and obstruction. How- ever, arterial conduits are more limited in their availability and ease of procurement compared with venous grafts, specifically the saphenous vein. Therefore, saphenous vein grafts (SVGs) remain the most commonly used conduits.
etiology of venous CABG graft complications
Early graft occlusion is primarily due to vascular damage that can occur at surgery, whereas vessel wall changes resulting from expo- sure to systemic blood pressure may predispose to occlusion in later stages.
general localization of grafts
A right SVG (a) is attached to the anterior aorta proximally and to the posterior de- scending artery distally. A left SVG (b) has an altered appearance because it is attached to the aorta with an aortic connector device (arrow); the origin of this SVG is moved laterally to prevent kinking. A typical left IMA graft (c) is left intact at its origin and grafted to the LAD artery distally.
early graft complications
- thrombosis
- malposition
- kinking
- spasm
- iatrogenic-dissection
- pl eff/pericardial eff
- infection
late graft complications
- occlusion
- aneurysm
Scimitar ass
ASD (70%)
right lung hypoplasia
right pulm a hypoplasia
Ebstein ass
ASD (50%)
ways of describing cardiac wall kinesis
normokinetic
hypokinetic
akinetic
dyskinetic
MR sequence for quantifying global and regional cardiac systolic function
SSFP
vertical long/2 chamber view-how to get it, what it shows, what it’s good for
- bisect BV and LV apex in axial view
- LV, LA, coronary sinus
1) wall motion/global LV function
2) MV issues-regurg, etc
3 chamber view/apical long/LVOT view
through aortic room in coronal
- LVOT tract
- MV, AV and IL walls
4 chamber view/horz axis
-lower 1/3 through MV & LV vertical long septal and lateral wall, apex LV RV free wall chamber size MV, TV
short axis
perpendicular to LV on 4 chamber view
-for quantification of ventricular volumes, size, mass and function
normal pressures for the heart chambers-RA, LA< RV, LV< PA< AV
RA: 1-8 LA: 4-12 RV: 15-30/1-8 LV: 100-140/4-12 PA: 15-30/4-12 AV: 100-140/60-80
carney complex
endocrine neo (pit)
- skin hyperpigm
- myxoma
rx papillary fibroelastoma
if syx
-consider valve sparing-regrowth s/p partial reection of valve
criteria to evaluate myocarditis
Lake Luise criteria: T2, EGE & LGE
-f/u: persistent edema/hyperemia=chronic
mcc 2˚ restrictive cardiomyopathy
amyloidosis
imaging amyloidosis
- concentric myocardial thickening (LV > RV, At, valves)–> atrial dilation
- diiffuse DGE
- darkened blood pool
signs of cardiac tamponade: Beck triad, pulses paradoxes, kussmaul sgx
- Beck triad: 1) hypoTN 2) (+) JVP 3) (-) HS
- pulsus paradoxus- (-) SBP (>12 mmHg) on inspiration
- kussmaul sgx: (+) venous distention and P on inspiration
ddx pericardial calcification
- uremia (viral)
- Tb
img dilated cardiomyopathy
- ED vol > 5.5 cm
- EF <40% (AICD < 35%)
- midwall enh (subtend if ischemia)
- heterog wall thickness, thinning, preserved RV mass
- linear midway septal stripe (DGE)-30%, subclinical foci myocardial ischemia, SCD (electrical pw)
restrictive vs constrictive cardiomyopathy
both char by impaired diastolic filling, identical Vt pressure tracings
- constrictive treated with surgery. Restrictive poor prognosis
- restrictive- pericardial thickening, diastolic septal bounce
Rx restrictive cardiomyoapthy
- decrease PL w/o CO (diuretics, NO)
- BB/CCB
- underlying dx
- PM/ICD/tx
post partum cardiomyoapthy
ddx of exclusion
- last mo-5 mo pp (80% w/i 3 mo
- EF < 45%
Iron overload cardiomyopathy
- hereditary-1˚ (AR), thalassemia
- 2˚
Iron overload cardiomyopathy-imaging
1) restrictive
2) dilated cardiomyopathy
- T2*-quantifies sev of Fe depot; powerful predictor, follow resp to rx (<20msec=sign Fe depo, <10msec-(+) risk CHF, arrhythmia.
- field inhomogeneity
- diffuse (inhomog) myo (epi –> mayo –> SE)
* <3 func preserved until critical storage cap reached –> rapid decompr
HCMO risk of SCD
1) thickness
2) perfusion abN
3) fibrosis
mc cardiomyopathy
HCM
HCM LVOT obstr
~25%
-basal septum HTr & SAM
myocardial noncompaction-patho, triad
- “spongiform cardiomyopathy”
- developmental defect in embryologic formation of LV-part of LV failure to form solid myocardium/papillary m
- dx: 3+ trab in 1 img plane OR 2.3:1 NC:comp
- triad: thrombus, stroke, CHF
- rx-if triad
myocardial noncompaction-img
- (+) LV trab, (-) kinesis –> (-) global Vt function
- BiVt enlargement
- LV thin wall
myocardial noncompaction-associations
- LVOT stenosis
- Ebstein
- TOF
- Barth syndrome
Barth syndrome
- cardiomyopathy
- skel mopathy
- growth retardation
- neutropenia
arrythmogenic cardiomyopathy-path
- familial/genetic 15-20% (AD>AR)
- fibrofatty replacement of Vt myocytes–> systolic contraction abN, aneurysm
arrythmogenic cardiomyopathy- img
- Regional RV a/dyskinesia/dyssynchronous RV contr
- RV EDV, ef < 40%
- RV thin wall, RV (+)
- LV(+) (3/4)-late dx, :(
- DGE
arrythmogenic cardiomyopathy-minor/major criteria
- RV enlargement
- focal aneurysm
- fat can be seen with aging
arrythmogenic cardiomyopathy-mx
ICD
catecholamine induced (takotsubo) cardiomyopathy
- apical ballooning
- hypokeniesia
- ø abn enh
LAA in rheumatic vs non rheumatic mitral regurg
enlarged in rheumatic causes of mitral regurg
Mitral valve prolapse-path
-myxomatous degeneration of leaflets –> thickening, redundancy; chordal elongation, annular dilation
Mitral valve prolapse-diagnostic criteria
1) 2+ mm beyond
2) classic = 5mm thick, non classic-<5mm
Mitral valve prolapse-complications
~1/4 people
- IE
- myocardial insuff
- stroke/systemic infarct
- arrythm
“severe” MR
<1 (N=4-6 cm2)
mitral annular calcification
- degenerative process, Ca depo on fibrous nannulus
- stroke, CV, afib
- marker of CV dx!
- ass w/ MR (vs mitral valve Ca–> MS)
Aortic stenosis heart size
LV HTr, no change heart size
grading aortic stenosis
- mild/mod/sev
- valve area: >1.5, 1-1.5, <1 cm2
- transvalvular vel: 2-2.9 , 3-3.9, 4+ m/sec
- mean P gradient: <20, 20-39, >40 mmHg
complications endocarditis
- dep on virulence
- cusp perforation
- chordal rupture
- valvular aneurysmal bulge
- perivalvular abscess
- fistula btw vess, chambers
- ext beyond valve (conduction system)
pulm edema after MI
poor prognostic factor
true vs false(pseudo) aneurysms
- true-focal outputting LV wall containing all m layers and ass with LAD occlusion. Can Ca. Medically mx.
- false-contained rupture, no myocardium involved. Ass w/ occ circumflex or RCA. Surgically repaired. MC upper diaph and pst wall
Dressler syndrome
autoimmune pericarditis s/ MI ass w/ pericardial/pleural effs
Loeffler cardiomyopathy
eusinophilic. acute necrosis
- Subendo DGE
causes of mid myo DGE
-dilated cardiomyopathy
-sarcoid
-chagas
-HCM
-restrictive CM
-ARCV
-Tako-tsubo
-
restrictive cardiomyopathy img
- pericardial thickening
- diastolic septal bounce
- normal Vt size
sarcoid cardiomyopathy
- restrictive cardiomyopathy
- LV dysfunction, arrythmia
- subepi, midmyo DGE in nodular/patchy pattern
-systolic anterior motion anterior leaflet MV-patho
via (+) vel and (-) P above valve –> LVOT obstr, MR
HCM img
- diastolic dysfunction
- abN LV myocardial thickening
- mid myo DGE
normal Vt thickness
8-12 mm
Thebesian valve
coronary sinus
Vieussens valve
coronary sinus & GCV
cardiac v’s
-middle cardiac v-pst IV (course w/ PDA in pst Vt groove)
crista terminalis
-sinus venous (smooth) vs RAA (trabecular)
Right & left atrial appendage locations
partially covers AV groove & RCA/LCA
infundibulum
conical pouch from which PV arise
right vs left ventricle
- thinner wall
- increased trab (esp towards apex)
moderator band
electrical conduction; septum –> free wall
TV
ant, pst, septal leaflets
-leaflets and pap m partially insert on septum
MV
- ant, pst leaflets –> cord tendinae –> papillary m –> lat & pst walls & apex LV
- D-shaped. ant leaflet thinner (<2mm), smaller.
- Pst=mural. ant=aortic (fibrous conn)
aortic valve divisions
- aortic ring –> annulus –> cusps –> sinus of valsalva –> sinotubular junction
- sinus of valsalva = dilated portion
2 papillary m’s in LV
- anterolateral-supp by LAD, LCx
- posteromedial- RCA (in R dom pts). rupture in MI via 1 supply
location of coronary sinuses
- R=ant
- L =left pst
- non-coronary= right pst
circle of vieussens
anastomosis of conus branch w/ LAD
how often does sinoatrial node ranch arise from Lcx?
42%
dose for PO metoprolol and sublingual nitroglycerin
- 5-25 mg
- 0.5-0.8 mg
Ca score
plaque burden (not stenosis) ->100 AU: 5x risk coronary events
significance of aberrant right subclavian in setting of thyroid surgery
-recurrent laryngeal n will not be in usual location
pathophys intramural hematoma
- vasa vasorum rupture
- htn, trauma
penetrating atherosclerotic ulcer
- focal intimal defect at site of atherosclerotic plaque
- desc thoracic
- hi rate rupture: >2cm diam, 1cm length
penetrating atherosclerotic ulcer vs simple ulcerated atherosclerotic plaque
penetrating-ext beyond expected contour of aortic wall
ductus diverticulum
- at aortic isthmus
- smooth broad shoulders, obtuse angle to wall
shape of mycotic aortic aneurysms
saccular
non-atherosclerotic causes of thoracic aortic aneurysm
- marfan, ehlers-danlos
- bicuspid aortic valve
- vasculitis-takayasu arteritis, giant cell arteritis, ankylosing spondylitis, relapsing polychondritis
- cystic medial necrosis
- infectious aortitis
what’s more common-asc vs desc atherosclerotic aortic aneurysms
descending
recommendations for surgery asc & desc thoracic aortic anuerysms and AAA
- asc: >5.5 cm (4.5 cm for CT do & BAV aortopathy)
- desc: >6 cm
- abd: >5.5 cm, syx
- annual growth >1cm/yr or 5mm/6 mo
early/impending aorta rupture sgx’s
- draped aorta sign-pst aorta draped along spine
- crescent-higher attenuation in lumen
complications TAA rx
- rupture
- dissection
- inf
- enkdoleak
- paraplegia (artery of adamkiewicz occlusion)
tulip bulb-shaped aorta
annuloaortic ectasia w/ effacement of sinotubular junction
how to measure aorta
double oblique reformatted images
US screening for AAA
- high risk > 65 yo
- <4cm: 6 mo f/u –> stable? –> annual
- 4-4.5cm: f/u 6 mo–> stable? –> 6 mo
- 5-5.5cm- consider sx
- > 5.5: surgery recommended
endovascular vs open AAA repair
-same long term outcomes, endovascular repair requires repeat interventions
complications AAA endovascular repair
- rupture
- dissection
- inf
- endolea
- aortoenteric fistula
endoleaks
- type I-inadequate graft seal (IA= =proximal, IB=distal)
- type II-persistent collateral flow to excluded aneurysm
- type III-device failure through graft fabric or segments of a modular graft
- type IV-pourous
- type V-endotension
known RF for type IA endoleak
conical thrombus containing neck at proximal EG attachment
type I endoleak
- inadequate seal at prox or distal ends
- early complication
- always repair (risk of rupture)
type II endoleak-moa
inflow (IMA) and outflow (lumbar) perfuse growing aneurysm
type III endoleak MOA
1) inadequate or ineffective sealing of overlapping comps of modular EG
2) complete sep of modular components
3) rupture or tear of EG fabric
- early-technical. Failure to adequately overlap modulator comps)
- later-device bd
pseudocoarctation
- focal narrowing of aorta
- sim to morphology of true coarctation but no pressure differential or collaterals
- ass w/ BAV, PDA, ASD, VSD
infantile coArc
- preductal –> LV obstr –> CHF
- archy hypoplasia
- no collaterals (no time to form)
SPIN echo imaging
- black blood, longer acquisition (better resolution), decreased metal artifact
- for anatomy
GRE echo
- faster (workhorse), metal artifact
- Vt function, valve dx, myocardial perfusion, delayed img, MRA, vel/flow
steady state free procession
- Cine.
- cardiac function and anatomy
- most reliable accurate aortic root measurement (ECG gated breath held cine img). Superior bc motion artifact not an issue AND both systolic and diastolic measurements are possible.e
- Fast GRE for cine
- high temporal resolution
- contrast btw myocaardium and blood
- wall motion and volumetric measurement. Standard for visually and objectively evaluating global and regional systolic function in both Vts
subepicardial enhacement
sarcoid
myocarditis
inversion recovery
- null myocardial signal to evaluate myocardial abN. Used in delayed enh.
- ~330msec
mech of DGE
- cell death
- abNo depo
interatrial septum normal width
3-4mm
stunned myocardium
- myocardium being perfused normally but not contracting–acute, just after MI
- near infarcted tissue
hibernating
- hypokinesis from decreased perfusion
- chronic. Viable and will reconstruct after perfusion.
- near scarring or remotely away
right vs left atrial appendages
R-trapezoidal w/ broad connection
L-tubular w/ narrow connection
atrioventricular discordance
R and L atria connect to L and R Vt respectively
ventriculoarterial
Aorta arising from morphological RV, PA arising from morphological LV
Transposition ass w/ atrioVt and Vtarterial transposition
- L type
- aorta will be anterior and to L of PA
ventricular rupture is ass w/ true or pseudoaneurysm
pseudo
upper limits normal for RV EDV
male: 100 mL/m2
female: 90
major criteria arrythmogenic right ventricular dysplasia
isolated RV aneuryms
massive global or segm RV dil
sev (-) RV EF w/ minimal involvement of LV
mx anomalous CA w/ inter arterial course
-unroofing (enlarge orifice of anomalous coronary)
normal thickness interVt septum
10-12mm
MC HCM variant
asymmetric septal hypertrophic variant
-dx= IV wall > 15mm and septal wall:free wall >1.5
grid taggin
visualize transmural myocardial mvmt to quantify local intramyocardial motion measures, its: strain and strain rate
moa Ebsteins
apical displacement of SEPTAL TV leaflet >20mm or 8 mm/m2
-ant and inf leaflets also abN with varying degrees of dysplasia and tethering
best imaging too for RV morph and function
MRI
-Echo hindered by retrosternal loc and complex geo
tricuspid atresia
hypoplastic Right ventricle
N sized heart, (-) pulm vasc
-muscular/fatty ridge in location of TV
-ass: 100% have ASD, VSD and 30% transposition
what is an overriding aorta?
aorta arises over a VSD rather than over the LV –> de-oxy and oxy blood circ
truncus arteriosis-pathophys, leaflets of TA, radiograph findings, classification scheme, mx
- pathophys: failure of truncoconal ridges to fuse –> failed division of TA into aorta and pulm a, defect in Vt septum.
- leaflets: 2-5 (3 MC)
- Rgx: R. arch, CMG, pulm vasc+
- Collett & Edward’s: var org PA from trunks (MC=type I: MPA arise from L pstlat asp
- sx: new pulm outflow tract w/ synthetic graft material (watch CA’s!)
mc cyanotic heart disease of newborn
transposition of GV
pathophys TOGV
failed clockwise rotation of of aorticopulmonary septum (which normally puts AV pst & R of PV)
tricuspid atresia: findings, ass, mx
-muscular fatty ridge of tissue in loc of TV sep large RA from hypoplastic RV.
+FO or ASD for flow into LA
+VSD for low into pulm circ
(-) pulm circ
- Ass: TOGV (MC), pulm stenosis
- Glenn (SVC –> pulm a), Fontan (RA –> pulm) + correction of intracardiac shunts or transposition
RV “atrialization”- what does it mean, consequence
- RV incorporated into RA
- this portion has abN thin wall –> tricuspid regurg
which leaflets are abnormally displaced in Ebstein anomaly?
septal & pst
Epstein appearance
Rgx: box shape (elongated, enlarged RA)
Ebstein ass
patent FO
secundum AsD
ECG abN
Li in early pregnancy
Rx TOF
surgical:
- palliative shunt (Blalock-Taussig)
- compplete repairr infundibular outflow obstr w/ patching of VSD (Lillehei procedure)
