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Stanford 1

QuestionAnswer
name 2 braided and 2 monofil nonabsorb sutures braided: silk, ethibond; monofil: prolene, nylon
name 4 absorb sutures chromic/plain gut, vicryl (braided), monocryl (monofil), PDS (monofil)
name 2 categories of lvls of evidence size of the effect (I-III), certainty/precision of tx effect (A-C)
describe categories for size of effect for EBM I: benefit >> risk, II: benefit>risk; III: risk> or = benefit
describe categories for certainty/precision tx effect for EBM A=mltpl RCTs or meta analysis (mltpl popul analyzed), B=1 RCT or mltpl nonRCTs, C=consensus opinion, case studies or std of care
indications for sx for asympt AS and lvl of evidence (4) Class IC: if severe AS w other sx or EF 50% or less; Class IIbC: severe AS w abnl response to exercise (can't incrsd SBP 20); Class IIaB: mod AS w other sx
periop mortality AVR, incl if also CABG 3-4% (STS database), 6% if also CABG
risk factors for rapid progression in AS >50yo, severe Ca++, CAD,
avg change in severe AS velocity jet and AVA change in velocity 0.3 m/s/yr, AVA 0.1 cm^2
describe Gorlin conundrum formula for AVA doesn't calculate AVA well in low flow states
better ways to assess AS in low flow states AV resistance and stroke work loss
likelihood severe asympt AS will be free of sympt 5y 50%
once sympt present in AS survival angina 3 yrs, symcope 2y, CHF 1.5y
term for pulse in AS parvus et tardus
Gorlin eqn CO/(HR x ejxn time x 44.3 x mean gradient)
describe Moore study on prosthetic pt mismatch in AVR affects survival if <70yo (although Dartmouth grp showed difft results if use geomet dimensions)
describe cutoffs for prosthetic pt mismatch severe EOA/BSA <0.65, moderate 0.65-0.85
cut offs for AS jet velocity, mean gradient, AVA jet velocity, gradient, AVA: mild= <3, <25, <1.5; severe= >4, >40, <1
what is the AVA index for severe AS <0.6
MC BAV Type I L-R (71% in Stanford study)--also assoc w coarct
genetics assoc w BAV eNOS thgt assoc, NOTCH involved in BAV and Ca++, ACTA2 SMaA famTAAA and dissections and BAV
% coarct w BAV 50-75%
Sievers Ross v AVR study used propensity matching and no diff survival and both same as general population--but Ross had more reoperations, no diff in thromboembol
Yacoub Ross v homograft study at 10yrs homograft did worse and transvalv gradient steadily incrsd; Ross did same as gen population
what % severe AS don't undergo surgery 30%
pts enrolled in Ib part of Partner trial severe AS AVA 0.8, grad 40, velocity 4, inoperable=10% STS risk score or predicted death 15% 30d; exclusion: >3 AR, BAV, no Ca++, EF <20%, CAD needing revasc
results Ib Partner 1 yr mortality 30.7% v 50.7%; 30d TAVI had higher stroke (5% v 1.1%) and vascular cxns (16.2 v 1.1%). 11% mod or severe paravalv regurg
which valve used Partner Sapien
cut offs for MS (mean gradient, PA SP, valve area) mean gradient, PA SP, valve area: mild <5, <30, >1,5; severe >10, >50, <1
what's nml MV area 4-5
timeline of MS s/p RhF 20-40y, once limiting sympt survival 0-15% 10y and once pul HTN mean survival 3yrs
indication for sx in MS Class IB NYHA III-IV mod or severe MS; CLassIC mod or severe MS + mod or severe MR; Class IIaC: severe MS + PASP >60, NYHA I-II
how much does MA contract and timing 20-40%, 89% occurs before LV cxn, which depends on strength and duration of atrial cxn
describe MV leaflet open and closure leaf open starts in ctr w edges still opposed, middle then commissures…leaf closure initiated by LA cxn
cut offs for AR (angio grade, vena contracta width, regurg vol, regurg %, ERO) (grade, VC width, regurg vol, regurg %, ERO): mild: 1+, <0.3, <30, <30, <0.1; severe= 3/4+, >0.6, 60, 50, 0.3
how does heart compensate for AR at sarcomere lvl sarcomere added in series so nml preload at sarcomere lvl, but incrsd wall stress (incrsd chamber size), also incrsd afterload leads to hypertrophy…so both P and vol overload
indications sx for AR Class I: sympt, chronic severe; chronic severe asympt if EF<50 (Class I) or ES >50 (Class IIb); if moderate AR and sx on asc Ao or CABG (Class IIb)
what's the name of bobbing head sign in AR de Musset sign
name of pulse in AR Corrigans pulse or water hammer P (bounding pulse)
name of murmur in AR Austin Flint (1836-1915, president of AMA 1884)
med tx for AR afterload reduction w ACEI/nifedipine to reduce SBP, but don't use if no HTN
describe what happens in IVC in AV fxn just before AV opens Ao root expansion helps leaflets open, NC (connected to fibrous part MVAC) expands least, also longitudinal expansion of root
describe what happens AV during ejxn ann cxn (NC least), while commissures continue to expand (Lansac found base cont'd to expand), LC and NC clockwise torsion, RC CC. amt of torsion predict dP/dt while EF predicted ann cxn
describe what happens AV during IVR ann cxn asymm, commissures symm, longitudinal compression, when min LVP decrses work shifted to L base
describe what happens AV during diastole just recoil
what's the diff dynamics and kinematics kinematics is 3D location, by understanding dynamics (constitutive eqns) given boundary conditions can solve for kinematics
types of MR by Carpentier classif I=nml leaflet motion , annular dilation or endocarditis; II=prolapse, floppy MV w chord elong/rupture; III=restricted motion, A=diastole, B=systole, in rheum A+B, IMR=B, DCM=B + annular dilation
% of CHF w FMR. % FMR s/p inferior MI 40% of CHF and 40% inferior infarct (bc PM pap displaced laterally)
causes of MR in W Countries 70% degen w prolapse, 20% ischemic w tenting, 2-5% ea endocarditis and rheym
cut off to consider MVP 2mm above annulus
cut offs MR (angio, VC width, MR vol, MR %, ERO) (grade, VC width, regurg vol, regurg %, ERO): mild: 1+, <0.3, <30, <30, <0.2; severe= 3/4+, >0.7, 60, 50, 0.4…same as AR exc upper end of VC width and ERO
indications sx for MR ClassIB: acute severe sympt, chronic severe sympt NYHA II-IV EF>30% and/or ES >55, asympt chronic severe EF 30-60% and/or ES >40; ClassIIaB: asympt chronic severe EF>60%, ES <40 if repair >90%
how much EF change s/p surgery decrs 10%
recurrence of MR after surgery IMR annuloplasty (95% + CABG) in Cleveland incrs 3/4+ MR from 13 to 28% at 6mos…similar for difft ring types and smaller rings don't help
LA and LV measurements that predict outcome LA vol >40 means severe MR and predicts A fib; LVESVI >30ml/m^2 poor outcome
how does MVP murmur change w loading midsys click w late sys murmur, incrsd w standing and valsalva, decrs w squatting (same as HOCM and opposite of MR), handgrip incrses MVP murmur and decrses HOCM
describe Crawford classif aneur I=desc thoracic, II=desc and infrarenal **highest risk paraplegia, III=distal desc and infrarenal, IV=infrarenal
describe deBakey classif I=asc and desc, MC and worst px, II=asc, III=desc (b if also infrarenal)
indication surgery TAAA TAV asc 5.5, desc 6.5; MFS/BAV asc 5, desc 6; LDS: 4.5…4.5 if AV surgery, >1cm/yr grwth, dissection
indications AAA surgery 5.5cm or 2x nml, >0.5cm/6mo, any sympt
types of endoleak I=seal (prox or distal), II=bw branch vessel and sneur sac, ie IMA or intercostal, III=through graft, IV=incrs size aneur sac endotension
preop mgmt of aneur/dissxn MAP 60-80, HR 60, metoprolol, no SNP (decrsd afterload incrses shear and dP/dt)…decrsd SBP is to prevent rupture and anti impulse (decrs dP/dt)
% dissxn w/o tear, how occurs 13% no tear, thgt intramural hematoma from bleeding of vasa vasorum
where dissxn tear in acute A R anterior and sprials
preop malperf acute A, how relates to mortality Mohr 2009, if preop malperf 30% early mortality (v 14%), cor malperf and visceral worst; 48% cor resolve incl 60% paraplegia
outcome for visceral malperf in acute A 75% in hospital mortality
overall mortality Acute A dissxn 1-2%/hr, used to be 50% 48h, now if make 24hr, 10-20% 2d-5d, then 1%/d
how many Acute A present w CP 15-20%
how many Acute A present w AI 75% but in 85% can save native AV
when take acute B dissxn to surgery if rupture or intractable pain. Rupture actually did not incrs risk cxns or mortality
op mortality Acute B Coselli 22% and 6% paraplegia
mgmt desc thoracic asympt and inoperable no TEVAR, Demers Stanford study 2004, 5yr TEVAR 31% v 78% if operable (no comparison no tx v TEVAR)
% aneur undiagnosed 85%
when is risk death highest s/p dissxn first 2 yrs
how many ppl get new aneury s/p dissxn 20% get new aneur from dilation of residual false lumen
who used cellophane to wrap aneur Abott and Paulin in 1949
name for cystic medial degen Erdheim dystic medial degen
BAV and types of arches I=Ao root (13%), II=incl tubular asc Ao (14%), III=tubular and trvrs (28%), IV=root, asc, trvrs (45%)
should BAV Ao be replaced sooner Class C, know BAV Ao abnl, grow more quickly, dissxn younger, but Yale study showed similar rate rupture, dissxn + better longterm survival (younger, healthier)…cxns not at smaller dia
endovascular v med tx for uncomplicated B dissxn INSTEAD trial showed no diff 2yr
how much do Ao expand s/p TEVAR 0.1cm/y asc, 0.3cm/yr desc and exacerbated by patent intercostals…tendency to dilate bc applies radial force
what % dissxn have MFS 5-9%
% of MFS sporadic mutation, overall incidence MFS up to 25%, overall incidence 1:5,000
who MFS named after, and when gene discovered Antoine Marfan Fr pediatrician in 1896 who noticed in little girl, gene discovered 1991
systemic features MFS arachnodactyly, high palate, jt hypermobility, flat feet, ectopia lentis, hernias, MVP, PTX, pectus, scoliosis
role of fibrillin in eye ciliary zonules
key diff Loeys Dietz and MFS hypertelorism, cleft palate/bifid uvula, aterial tortuosity, club feet, thin velvety skin w easy bruising, more diffuse medial degen
mutation in LDS and how relates to TGFb signaling TGFbR1,2 but increasd pSMAD2 suggests TGFb signalling is upregulated
what rescues phenotype LDS in mice losartan by blocking TGFb
how freq famTAA in TAA, genetics 19% TAA have 1st degree relative w TAA, present younger, assoc w TGFbR1,2; ACTA2, if also PDA assoc w MVHII
what's arterial tortuosity syn? Genetics AR glu transporter mutated (SLC2A10) and incrsd TGFb; they have facial dysmorphism
mutation in Ehlers Danlos IV vascular type of Ehlers Danlos, mutation Col III have pale translucent skin
decsribe kyphoscoliosis type of Ehlers Danlos type VI, due to lysyl hydroxylase mutation, fragile eyes and mscl wknss, very rare
name 3 other syndromes w FBN mutations 1) Shprintezene Goldberg (craniostenosis, MR; FBN1 and others); 2) Weille Marchesani (spherophakia round eyes, brachydactyly, stiff jt; FBN1); 3) Congen contractural arachno (crumpled ears, contractures; FBN2)
describe features and genetics of homocystinuria AR defect cystathionine synthase defic, Marfanoid w/o arachnodactyly, dwnwrd subluxation, hypercoag, MV/AV regurg w/o Ao dilation, MR, scoliosis, large stiff jts, often blond, blue eyed
dx and tx homocystinuria dx: decrsd methionine in urine and blood, tx B6 cofactor helps convert homocysteine to cystathionine, diet restrict methionine, ASA
Created by: ehstephns on 2011-04-24



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