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Stanford 2

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name 5 CABG studies   SoS (surgery v bare stent), SYNTAX (DES), CASS, MASSII (single institut med v PCI v CABG), COURAGE (initial PCI v med and delayed PCI), FREEDOM (DES for DM)  
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results SoS CABG trial   2002, CABG did better than bare metal stents  
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results SYNTAX trial   DES incrsd major cardiac or CVA, mostly due to need revascularization, no diff repeat MI or survival, incrsd stroke in CABG  
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results CASS trial   3 vessel EF <50% benefit CABG  
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results MASSII trial   single institution, composite mortality, Q wave MI, revasc. CABG best then PCI then med (but med subopt w 1/3 not on statin 80% ASA although maybe this is realistic compliance)  
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results COURAGE trial   no diff initial PCI v med and deferred PCI, based on this for ppl nml EF only revasc if sympt refractory to med…MASSII suggests differently and sicker ppl  
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ESC 2010 guidelines revasc   L main: CABG (Class IA), 1-2 vessel and prox LAD (ClassIA) but if no prox LAD PCI (CLassIC)  
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structures around NC sinus   LA, RA, transverse sinus  
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structures around RC sinus   RA, RVOT  
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structures around LC sinus   LA  
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structures NC/RC interleaf triangle   membranous septum, AV conduction, TV septal leaf also R fibrous trigone  
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structures NC/LC interleaf triangle   subAo curtain/MVAC  
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structures LC/RC interleaf triangle   L fibrous trigone, muscular septum/infundibulu,. Pul  
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structures around MV in MVR   great cardiac vein, cirumflex artery in anterior area, conduction bundle, cor sinus and AV nodule artery along PM pap side  
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blood supply for PM pap? Anterolat pap?   PM Pap=RCA, AL pap=LAD and LCx  
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branches off Lmain, RCA   Lmain: Lcx->OM, LAD->diag; RCA: marg, PDA  
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internal thoracic/I mammary comes off? Thyrocervical gives off?   mammary comes off subclavian, thyrocervical br is after mammary and gives off I thyroid artery  
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course of vagus   on R the R recurrent laryngeal hooks R subclavian, L runs w LCCA and L recurrent hooks at lig arteriosum  
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recurrent laryngela innerv   all mscle of larynx involved in vocal folds exc cricothyroid (ext br of S laryngeal n)  
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if injury vagus, ie innerv of vagus   dysphagia, uvula, baroreceptors  
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innerv phrenic, course   lateral to vagus runs along scalene (whereas vagus in carotid sheath), innerv C3,4,5 and diaphragm  
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innerv that gives voice strength   ext br of s laryngeal n that innervates cricothyroid  
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branches of celiac   L gastric, c hepatic (cystic, hepatic, R gastric, gastroduo), splenic  
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branches of SMA   ileocolic, R and mid colic  
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branches of IMA   L Colic, sigmoid, rectal  
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order of branches off abd ao   celiac, SMA, renals, IMA, then branch of iliacs  
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branches iliacs   c iliac: internal iliac (pelvic vessels), ext iliac (gives off inferior epigastric), then becomes femoral when passes inguinal lig, gives off deep femoral, then becomes popliteal at Hunter's canal (gives A tibial (dorsalis pedis), P tibial, peroneal)  
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anastomoses bw SMA and IMA   marginal artery  
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anastomoses bw celiac and SMA   pancreatic and duo  
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what are Riolan's anastomoses   anastomoses bw m colic (SMA) and L colic (IMA)  
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s thyroid a comes off? I thyroid?   s thyroid a off ext carotid, I thyroid comes off thyrocervical trunk off of subclavian  
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order of cartilage in neck for tracheostomy   hyoid, then thyroid cartilage, then cricoid  
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what's Jackson triangle   sternal notch, SCM, and cricoid  
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eqn for DavidV Stanford modified   David and Feindel eqn, D=hgt leaf x 2 x 0.67 + 2 x Ao wall then use 6-8mm bigger  
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what's penninsula style arch   just replace the underside of the head vessels  
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non-everting suture v everting   non everting is strongest use w bioprosthetic and Starr, goes from ventricular side to atrial. Everting (atrial to ventricle) used in mech  
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how orient mech valve   struts are S-L so don't trap chordae  
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story of pyrolitic carbon   used in inner wall of Tokamak, hi vaporization temp and doesn't activate under bombardment of neutrons. Dr. Bokros read a Gott article abt using carbon based paint to coat artificial heart components in 1966  
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how measure MVR   for IMR/FMR measure bare areas, for MVP measure complete AML. Odd  
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types of Sondergaard interatrial groove incisions   std vertical L atriotomy, extended transeptal biatrial, Khonsari oblique biatrial  
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what's eqn Nyquist limit   freq > 1/2 PRF (ie  
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describe torsion of LV   base moves clockwise and apex counterclockwise, as untwist it helps LV fill  
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describe E, A wave on transmitral flow   E is rapid early ventricle filling from P gradient as LV relaxes, A= atrial cxn  
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what's B bump on transmitral flow   from incrsd LVDP MV closure is earlier/interrupted  
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what happens to Echo when diastolic dysfxn Grade I   delayed MV open, E wave lower amp and broader (E/A <1 and decel >240ms)  
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describe pseudonml in LV diastolic dysfxn   LV stiffens makes relax worse so rely more on atrial cxn w incrsd LA P which restores LA-LV gradient…if E/A decrses by 50% during Valsalva you've unmasked restrictive filling (shouldn't change)  
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what happens in Grade III LV dias dysfxn   incrsd LA P leads to E w higher amp but shorter bc incrsd LV P, low A wave (failure LA cxn), E/A >2  
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what happens to septal motion s/p any cardiac surgery   exaggerated anterior motion of hwole heart, usu just noted abnl anterior motion of septum, but shouldn't see any changes in thickening  
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how is CO calculated using Echo   CSA x TVI  
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how is MPI calculated   myocardial perform index = time isovol relax / ejxn time .  
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what's a nml MPI and how does it change w sys and diastolic dysfxn   nml <0.4; dias dysfxn incrsd relax time --> MPI incrses; sys dysfxn decrsd ejxn time --> MPI incrses  
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which measures of LV fxn are afterload dependent? Afterload inde?   afterload dependent: SV, fractional shortening; afterload inde: LV wall stress (takes into acct P), P-V loops, and dP/dt  
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how is wall stress calculated   wall stress = P x radius / wall thickness  
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how can color doppler be misleading in terms of MR   1) the MR jet will include RBCs in LA being pusched by jet; 2) large low veolocity jet can appear smaller bc low velocity  
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advantage/disadv of pulsed v continuous doppler   pulsed can tell exactly where the velocity is coming from but can have aliasing, continous don't have aliasing but can't tell exactly where velocity is  
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what's more sensitive/early indicator of dysfxn than wall thickening   strain and strain rate  
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bernoulli eqn   pressure gradient = 4 (velocity)^2 …as long as proximal velocity is low  
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describe pressure recovery and when do you see in Ao?   as go thru stenotic valve PE is converted to KE, once thru KE converted back to PE so P incrses and velocity decrses (most likely to happen if <3cm dia Ao)  
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advantage of continuity eqn and assumptions   unaffected by regurg of LV dysfxn, assumes blood noncompressible and conduit inelastic  
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how use continuity eqn for calculating AVA   measure TVI and CSA at one spot and TVI at 2nd spot and can solve for CSA  
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how does P t 1/2 change for MS   P t 1/2 depends on P gradient bw LA and LV and is time for peak vel = peak/(sqrt2) = 0.7 peak …as MS incrses P t1/2 incrses  
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as AS gets worse how does the velocity profile change   peak vel becomes later and more rounded in shape  
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eqn AV resistance   mean P gradient / mean flow rate x 1333 OR 28(sqrt mean gradient)/ AVA  
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eqn AV stroke work loss   100 x mean P gradient / (mean P gradient + SBP)  
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3 tx for low CO   epi (unless arrhyth, tachy), dopa if low SVR, dobutamine if high SVR  
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what's nml SVR and how calculate   900-1300, 80*(MAP-CVP)/CO  
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nml wedge   5-12 mmHg  
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nml PA P   15-30 / 5-12  
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how tx low BP low SVR   Levo, or vasopresin if that doesn't work  
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general mgmt low CO   optimize preload (PCWP 18-20) then optimize afterload  
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role alpha1 receptors   vascular cxn  
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role alpha2 receptors   decrs symp, decrs insulin  
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role beta1 receptors   incrsd HR and contractility, incrsd renin  
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role beta2 receptors   vasodilate, incrsd HR and contractility (less so than beta1), incrsd glucneogen, bronchodilate  
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role D1 receptors   relax renal vascul  
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role V1, V2 receptors   V1=vascular cxn, V2=water reabsorb  
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different roles of dopa depending on dosages   2-3 renal dose-vasodilation decrs BP; 3-8 B1 mostly incrs HR, >8 alpha incl incrsd NE, incrsd SVR, incrsd filling P and LV fxn  
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role of epi   alpha1,2 and beta1,2; at low dose just b1. alpha1 incrses SBP, b2 decrses DBP, overall MAP no change, incrsd HR from B1. risk arhyth and metabolic acidosis, incrsd lactate and decrsd splanchnic perfusion  
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role of NE/levophed   alpha1,2 >b1. alpha incrses SVR and BP, b1 incrses HR and contractility, not much incrs CO. good for septic shock low BP low SVR. Not for ischemia or CHF. Decrses renal BF at high doses.  
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role of dobutamine   mostly b1, some alpha1, beta2. unlike dopa incrses myoperfusion, grtr incr HR relative to epi. Also pulmon vasodilat synergistic w milrinone  
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role of milrinone (Primacor)   PDEIII inhib incrses cAMP incrses Ca++ uptake and LV relax. Decrses SVR and pul VR, inotropic, decrses SBP some incrs HR, decrs cor vascular resistance **don't use hypotension  
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how does CaCl fxn in CICU   incrsd SVR, incrsd MAP, no change in HR  
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how does digoxin work   cardiac glycoside from foxglove, Na/K ATPase incrses Ca++. Can cause thrombosis of mesenteric veins. Sl inotrope, peripheral vasodilation, mild diuretic in CHF w incrsd renal BF  
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Rx that incrs dig levels   QUACCS=quin, amio, cimetidine, CCB, spiriono  
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role Flolan   PGI2 endothel cells G Protein signalling, pul dilation w/o decrs SVR  
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role Sildanefil (Revatio)   pulHTN, PDE5 (mostly arterial SMCs in lung) cGMP  
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role nesiritide   recombinant BNP, counters renin system, works via cGMP to SMC relax-->vasodilation, natruiesis, diuresis, incrses CO w/o incrsd HR or myocardial demand  
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