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Stanford 2

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)
results SoS CABG trial 2002, CABG did better than bare metal stents
results SYNTAX trial DES incrsd major cardiac or CVA, mostly due to need revascularization, no diff repeat MI or survival, incrsd stroke in CABG
results CASS trial 3 vessel EF <50% benefit CABG
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)
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
ESC 2010 guidelines revasc L main: CABG (Class IA), 1-2 vessel and prox LAD (ClassIA) but if no prox LAD PCI (CLassIC)
structures around NC sinus LA, RA, transverse sinus
structures around RC sinus RA, RVOT
structures around LC sinus LA
structures NC/RC interleaf triangle membranous septum, AV conduction, TV septal leaf also R fibrous trigone
structures NC/LC interleaf triangle subAo curtain/MVAC
structures LC/RC interleaf triangle L fibrous trigone, muscular septum/infundibulu,. Pul
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
blood supply for PM pap? Anterolat pap? PM Pap=RCA, AL pap=LAD and LCx
branches off Lmain, RCA Lmain: Lcx->OM, LAD->diag; RCA: marg, PDA
internal thoracic/I mammary comes off? Thyrocervical gives off? mammary comes off subclavian, thyrocervical br is after mammary and gives off I thyroid artery
course of vagus on R the R recurrent laryngeal hooks R subclavian, L runs w LCCA and L recurrent hooks at lig arteriosum
recurrent laryngela innerv all mscle of larynx involved in vocal folds exc cricothyroid (ext br of S laryngeal n)
if injury vagus, ie innerv of vagus dysphagia, uvula, baroreceptors
innerv phrenic, course lateral to vagus runs along scalene (whereas vagus in carotid sheath), innerv C3,4,5 and diaphragm
innerv that gives voice strength ext br of s laryngeal n that innervates cricothyroid
branches of celiac L gastric, c hepatic (cystic, hepatic, R gastric, gastroduo), splenic
branches of SMA ileocolic, R and mid colic
branches of IMA L Colic, sigmoid, rectal
order of branches off abd ao celiac, SMA, renals, IMA, then branch of iliacs
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)
anastomoses bw SMA and IMA marginal artery
anastomoses bw celiac and SMA pancreatic and duo
what are Riolan's anastomoses anastomoses bw m colic (SMA) and L colic (IMA)
s thyroid a comes off? I thyroid? s thyroid a off ext carotid, I thyroid comes off thyrocervical trunk off of subclavian
order of cartilage in neck for tracheostomy hyoid, then thyroid cartilage, then cricoid
what's Jackson triangle sternal notch, SCM, and cricoid
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
what's penninsula style arch just replace the underside of the head vessels
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
how orient mech valve struts are S-L so don't trap chordae
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
how measure MVR for IMR/FMR measure bare areas, for MVP measure complete AML. Odd
types of Sondergaard interatrial groove incisions std vertical L atriotomy, extended transeptal biatrial, Khonsari oblique biatrial
what's eqn Nyquist limit freq > 1/2 PRF (ie
describe torsion of LV base moves clockwise and apex counterclockwise, as untwist it helps LV fill
describe E, A wave on transmitral flow E is rapid early ventricle filling from P gradient as LV relaxes, A= atrial cxn
what's B bump on transmitral flow from incrsd LVDP MV closure is earlier/interrupted
what happens to Echo when diastolic dysfxn Grade I delayed MV open, E wave lower amp and broader (E/A <1 and decel >240ms)
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)
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
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
how is CO calculated using Echo CSA x TVI
how is MPI calculated myocardial perform index = time isovol relax / ejxn time .
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
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
how is wall stress calculated wall stress = P x radius / wall thickness
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
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
what's more sensitive/early indicator of dysfxn than wall thickening strain and strain rate
bernoulli eqn pressure gradient = 4 (velocity)^2 …as long as proximal velocity is low
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)
advantage of continuity eqn and assumptions unaffected by regurg of LV dysfxn, assumes blood noncompressible and conduit inelastic
how use continuity eqn for calculating AVA measure TVI and CSA at one spot and TVI at 2nd spot and can solve for CSA
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
as AS gets worse how does the velocity profile change peak vel becomes later and more rounded in shape
eqn AV resistance mean P gradient / mean flow rate x 1333 OR 28(sqrt mean gradient)/ AVA
eqn AV stroke work loss 100 x mean P gradient / (mean P gradient + SBP)
3 tx for low CO epi (unless arrhyth, tachy), dopa if low SVR, dobutamine if high SVR
what's nml SVR and how calculate 900-1300, 80*(MAP-CVP)/CO
nml wedge 5-12 mmHg
nml PA P 15-30 / 5-12
how tx low BP low SVR Levo, or vasopresin if that doesn't work
general mgmt low CO optimize preload (PCWP 18-20) then optimize afterload
role alpha1 receptors vascular cxn
role alpha2 receptors decrs symp, decrs insulin
role beta1 receptors incrsd HR and contractility, incrsd renin
role beta2 receptors vasodilate, incrsd HR and contractility (less so than beta1), incrsd glucneogen, bronchodilate
role D1 receptors relax renal vascul
role V1, V2 receptors V1=vascular cxn, V2=water reabsorb
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
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
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.
role of dobutamine mostly b1, some alpha1, beta2. unlike dopa incrses myoperfusion, grtr incr HR relative to epi. Also pulmon vasodilat synergistic w milrinone
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
how does CaCl fxn in CICU incrsd SVR, incrsd MAP, no change in HR
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
Rx that incrs dig levels QUACCS=quin, amio, cimetidine, CCB, spiriono
role Flolan PGI2 endothel cells G Protein signalling, pul dilation w/o decrs SVR
role Sildanefil (Revatio) pulHTN, PDE5 (mostly arterial SMCs in lung) cGMP
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
Created by: ehstephns