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CARDIOVASCULAR MCQ 1. a. b. c. d. e. What is the best prognostic indicator for pregnanc in a patient in the first tri!ester "ith !

itra# stenosis$ s !pto!s prior to pregnanc #ong !%r!%r disp#aced ape& beat #o%d !%r!%r MVA'(.) c!*

*. A !a#e patient+ on a!iodarone *(( !g dai# + "ho is post ! ocardia# infarct and has V, resistant to sota#o#. -o" has ne%ropath fro! the a!iodarone . "hat do o% do ne&t$ a. b. c. d. e. 2. a. b. c. d. e. contin%e a!iodarone *(( !g dai# and add p rido&ine stop a!iodarone for / da s and decrease to 1(( !g 0 da decrease a!iodarone to 1(( !g dai# stop a!iodarone for / "ee1s+ then restart 1(( !g 0 da change to f#ecainide R%nner "ith pa#pitations. 3C4 sho"n5 "enc1ebach. What ne&t$ Insertion of per!anent pace!a1er coronar angiograph reass%rance Stress 3C4 stress tha##i%!

/. 6ress%re trace 7%estion5 e#der# !a#e+ histor of heart fai#%re+ one episode of s ncope+ a fe" episodes of p%#!onar oede!a resistant to #asi& and digo&in. Started on captopri#+ had s ncope+ press%re tracing sho"n 8#eft 9entric%#ar press%re %p to *((+ aortic press%re 1*(0:(;. What is the best !anage!ent$ a. b. c. increase fr%se!ide ba##oon 9a#9%#op#ast aortic 9a#9e rep#ace!ent.

<. =o%ng */ ear o#d !a#e+ sa" LMO+ fo%nd to ha9e 10) s sto#ic !%r!%r+ >6 1*(0?(. 3C4 sho"n5 sin%s rh th!+ LV@ on 9o#tage criteria+ Q in III+ , "a9e in9ersion in aVL. Diagnosis5 a. b. c. d. @OCM nor!a# coarctation of aorta bic%spid aortic 9a#9e

). =o%ng !a#e "ho "as at "or1+ pre9io%s# "e##+ s%dden# co##apsed. >6 :(0/(. @ad contin%o%s s sto#ic !%r!%r "ith diasto#ic accent%ation. Catheter perfor!ed5 RA sat "as <<A RA press%re : RV :<A 6A :<A RV press%re /( "edge sat B<A Wedge press%re ? LV B<A LV press%re :(01* 6A press%re /( What is the ca%se$ a. b. c. d. VSD and Aortic inco!petence ASD dissection right sin%s of 9a#sa#9a r%pt%re

e. ?. a. b. c. d. e.

coarctation of aorta =o%ng !a#e "ith broad co!p#e& tach cardia after drin1ing a#coho#. >6 1((0?( @o" "o%#d o% treat$ #ignocaine i9 digo&in f#ecainide adenosine carotid sin%s !assage

:. Ma#e ad!itted "ith pain in nec1 "ith /( !!@g >6 difference. 8C#inica# pict%re of dissection;. >est !anage!ent$ a. b. c. d. e. beta b#oc1er and nitrate anticoag%#ate thro!bo# sis d %rgent angiogra! c#ose obser9ation.

B. Lad "ith h pertension for in9estigation+5 CD 2.*+ %rinar adrena#ine of <((+ %rinar noradrena#ine of ?((. -e&t in9estigation$ a. b. c. C, adrena#s 9eno%s sa!p#ing of adrena#s angiogra!

1(. Midd#e aged !an #ong histor of increasing d spnoea+ orthopnoea+ 6-D and an1#e oede!a. 3&a!ination confir!s CCE. CFR sho"n G ca#cified pericardi%!. Cardiac catheterisation is #i1e# to sho"5 a. b. c. d. e. f. giant CV "a9es e7%a# RV and LV s sto#ic press%res e7%a# RA and 6CW press%res RV diasto#ic press%re H LV diasto#ic press%re 6CW6 "ith inspiration ear# diasto#ic fi##ing

11. <) ear o#d "ith ischae!ic chest pain. S!o1er+ CC :((. 4i9en t6A "ith rapid decrease in s !pto!s. Q "a9es and idio9entric%#ar rh th!. What "o%#d o% see on angiograph $ a. b. c. d. Occ#%ded #eft circ%!f#e& Occ#%ded LAD "ith poor LV f%nction ?(A LAD and /(A circ%!f#e& and /(A RCA -or!a# LAD+ occ#%ded RCA.

1*. a. b. c. d. e.

With respect to esti!ation of diasto#ic heart fai#%re "hich of the fo##o"ing state!ents are tr%e5 re9ersa# of the 30A ratio is a co!!on finding in e#der# patients diasto#ic heart fai#%re is %s%a## absent in significant i!pair!ent of s sto#ic f%nction esti!ation of s sto#ic f%nction 8eIection fraction !eas%re!ents; corre#ate better "ith s !pto!s of d spnoea than esti!ates of diasto#ic f%nction ! ocardia# fibrosis is a significant contrib%tor to red%ction in co!p#iance red%ced diasto#ic f%nction d%ring the rapid fi##ing phase is d%e dependent acti9e ! ocardia# re#a&ation in o9era## cha!ber to red%ced energ

12. a. b. c. d. e.

With respect to coronar 9ein graft disease ear# graft fai#%re of appro&i!ate# 1(A in the first ear postGs%rger is d%e to acce#erated athero!a in the postGoperati9e period at ten ears post coronar b pass grafting abo%t ?(A of patients "i## not sho" !aIor disease progression in the b pass grafts aggressi9e LDL #o"ering "ith statin dr%gs has been doc%!ented to res%#t in red%ction of disease progression in coronar b pass grafts. screening patients "ith b pass grafts greater than ten ears o#d "ith e&ercise testing "o%#d be e&pected to ha9e a #o" rate of detection of rec%rrent disease a## patients after coronar b pass s%rger sho%#d be treated "ith a @M4GCoA red%ctase inhibitor

1/. A )( o fe!a#e had an ac%te ! ocardia# infarction 1* !onths ago+ fo##o"ing "hich she had #ifeGthreatening 9entric%#ar tach cardia. She has been noted to ha9e 9er poor LV f%nction. On *(( !g per da of a!iodarone+ "hich has been contro##ing the arrh th!ias+ she has de9e#oped a periphera# ne%ropath . ,he ne&t step in her !anage!ent5 a. b. c. d. Decrease dose to 1(( !g od after stopping for / "ee1s Lea9e *(( !g and add p rido&ine Change to f#ecainide Decrease to 1(( !g i!!ediate#

1<. A o%ng !a#e "ith recent 9ira# i##ness co!p#ains of pa#pitations. @e is fo%nd to ha9e a s sto#ic !%r!%r and an 3C4 is sho"n LV@ b 9o#tage criteria+ high ta1eGoff V#+ V2+ I+ aVL. ,he !ost #i1e# diagnosis is5 a. b. c. d. e. -or!a# 9ariant @ pertrophic cardio! opath Di#ated cardio! opath 6ericarditis Aortic stenosis

1). A fit /( o !a#e presents "ith pa#pitations. An 3C4 is ta1en d%ring s#eep sho"s Wen1ebach and rate H/(0!in. =o%r !anage!ent "o%#d be5 a. b. c. d. e. Insertion of pace!a1er Reass%re 6erfor! 36S coronar angiograph b#oc1er

1?. A cardiac catheter st%d is sho"n of an e#der# !a#e "ith increasing episodes of CCE. @e "as tria##ed on an AC3 inhibitor and e&perienced preGs ncope. ,he carotid p%#se is noted to be di!inished. 8Cath tracing sho"s #arge LV to aortic gradient 1(( !!@g at pea1+ on# one heart beat sho"n b%t 3C4 sho"s an ectopic;. ,he best !anage!ent "o%#d be5 a. b. c. d. Aortic 9a#9e rep#ace!ent b#oc1er >a##oon aortic 9a#9%#op#ast Er%se!ide

1:. An 3C4 is sho"n "ith a "ide co!p#e& tach cardia. 6atient is conscio%s "ith s#ight# #o" >6. @istor of a#coho# %se is gi9en. 3C4 contro9ersia# 8either AE "ith aberranc + or V,;. ,he best treat!ent "o%#d be5 a. b. c. Carotid sin%s !assage Adenosine E#ecainide

d. e.

Lignocaine i9 Digo&in

1B. A o%ng !a#e e&periences s%dden onset of chest pain on #ifting. >6 :(0/(. Contin%o%s !%r!%r "ith diasto#ic accent%ation. Catheter st%d sho"n5 Sats 6ress%res RA <<A : RV :<A /( 6A :<A /( "edge B<A ? LV B<A :(01* ,he !ost #i1e# diagnosis$ a. b. c. d. e. *(. a. b. c. d. *1. a. b. c. d. e. VSD D AR R%pt%red sin%s of Va#sa#9a ASD dissection coarctation In "hich of the fo##o"ing sit%ations "o%#d it be !ost appropriate to %se adenosine5 Asth!atic "ith a narro"Gco!p#e& tach cardia // o !a#e in AE "ith no histor of heart disease <: o !a#e "ith pre9io%s infarct and narro"Gco!p#e& tach cardia 6atient "ith I@D and "ideGco!p#e& tach cardia A o%ng person is described "ith 3C4 sho"ing "ideGco!p#e& AE. Which of the fo##o"ing "o%#d o% %se5 Digo&in Verapa!i# Adenosine E#ecainide Metopro#o#

**. A patient s%ffers an infarct+ "ith 3C4 sho"ing S, e#e9ation V*GV<. Short# after recei9ing t6A+ there is a short r%n of 9entric%#ar tach cardia b%t then the S, seg!ents ret%rn to base#ine. ,he !ost #i1e# findings on coronar angiogra! are5 a. b. c. d. e. 6artia# occ#%sion RCA ?(A LAD stenosis and /(A circ%!f#e& and RCA stenosis Co!p#ete occ#%sion LAD "ith poor LV f%nction 6artia# circ%!f#e& occ#%sion Se9ere trip#e 9esse# disease

*2. A o%ng fe!a#e presents in first tri!ester of pregnanc "ith !itra# stenosis. Which of the fo##o"ing is the best predictor of o%tco!e$ a. b. c. d. e. */. Length of the !%r!%r 6reGpregnanc s !pto!s Va#9e area on echocardiograph Disp#ace!ent of ape& beat Se9erit of s !pto!s Which of the fo##o"ing is !ost #i1e# to pro#ong the Q, inter9a#$

a. b. c. d. *<. a. b. c. d. e.

Lo" CD @igh Ca*D E#ecainide Digo&in Concerning cardio9asc%#ar ph sio#og 5 Difference in arteria# and 9eno%s o& gen sat%ration is in9erse# proportiona# to b#ood f#o". Va#9e area in aortic stenosis is proportiona# to the s7%are of the press%re gradient across the 9a#9e. 6eriphera# 9asc%#ar resistance is pri!ari# deter!ined b resting arteria# tone. -itric o&ide sti!%#ates adhesion of p#ate#ets to the 9asc%#ar endothe#i%!. Adrenergic acti9it increases ! ocardia# contracti#it 9ia an increase in c4M6 #e9e#s "ithin the ! oc te #eading to an increase in intrace##%#ar ionised ca#ci%!. Concerning atherosc#erosis O&idation of LDL in the b#oodstrea! is necessar for foa! ce##s to for! A 9asoconstrictor rather than a 9asodi#ator response to endothe#ia# d sf%nction indicates acet #cho#ine A deficienc of nitric o&ide has been !eas%red in atherosc#erotic p#a7%es ,he absence of s!ooth !%sc#e ce## pro#iferation indicates it is pri!ari# a disease of the inti!a 6#a7%es are !ore #i1e# to r%pt%re if the are concentric Mitra# reg%rgitation5 after#oad ! ocardia# O* cons%!ption Circ%!ferentia# LV shortening S sto#ic anterior !otion associated "ith !itra# 9a#9e pro#apse Associated "ith MarfanJs Which of the fo##o"ing are associated "ith hae!od na!ic co!pro!ise in SV,$ Long Q, 6 "a9e !orpho#og 6 G QRS dissociation QRS "idth Ventric%#ar rate 6regnanc ind%ced h pertension5 Is ca%sed b the trophob#ast Associated "ith increased intra9asc%#ar 9o#%!e In9o#9es genetic predisposition Is !ore #i1e# in o%ng pri!igra9ida Increased pressor sensiti9it @OCM associated "ith FG#in1ed recessi9e 9entric%#ar 9o#%!e 6%#!onar 9eno%s congestion Diasto#ic d sf%nction Abnor!a# ! osin

*). a. b. c. d. e. *?. a. b. c. d. e. *:. a. b. c. d. e. *B. a. b. c. d. e. 2(. a. b. c. d. e.

21. a. b. c. d. 2*. a. b. c. d. e. 22. a. b. c. d. e.

6har!aco1inetics in CCE If high hepatic e&traction c#earance If #o" hepatic e&traction ora# a9ai#abi#it IV ad!inistration prod%ces 9o#%!e of distrib%tion binding to a#b%!in Which of the fo##o"ing is not consistent "ith p%re diasto#ic d sf%nction$ 3#e9ated end diasto#ic press%re Cha!ber of nor!a# siKe. Abnor!a#GsiKed heart on &ra Ma be part of an t pe of #eft 9entric%#ar disease Red%ced eIection fraction With regard to ! ocardia# infarction+ "hich of the fo##o"ing state!ents is incorrect$ Right 9entric%#ar infarcts are "ith red%ced !orbidit and !orta#it rates co!pared "ith #eft 9entric%#ar e9ents Indi9id%a#s "ith an inferior infarct ha9e a red%ced 2(Gda !orta#it + co!pared "ith those s%ffering anterior infarctions In patients "ith a rightGsided infarct in "ho! there is ear# re9asc%#arisation of the infarctGre#ated arter + inG hospita# !orta#it is considerab# #ess than in patients "ho are not ade7%ate# reperf%sed. In right 9entric%#ar infarction there is a !ar1ed i!pro9e!ent in hae!od na!ic arid !echanica# para!eters of right 9entric%#ar infarction fo##o"ing re9asc%#arisation in contrast "ith #eftGsided ! ocardia# infarction Morta#it fo##o"ing nonGQ "a9e infarction is significant# red%ced in patients treated "ith betaGb#oc1ade.

2/. ,he inherited #ong Q, s ndro!e is characterised b a histor of s ncope arid s%dden cardiac death. Regarding the genetic basis of this disorder+ "hich of the fo##o"ing state!ents is incorrect$ a. b. c. d. e. ,his s ndro!e !a be associated "ith congenita# b#indness 6otassi%! s%pp#e!entation corrects the repo#arisation abnor!a#it in so!e cases of the #ong Q, s ndro!e. ,he #ong Q, s ndro!e !a be associated "ith an abnor!a# potassi%! channe#. Long Q, s ndro!e !a be ca%sed b !%tations in cardiac sodi%! channe#s. Ac7%ired and inherited #ong Q, s ndro!es !a both ca%se 9entric%#ar arrh th!ias arid !a ha9e a si!i#ar !o#ec%#ar basis.

2<. Ea!i#ia# h pertrophic cardio! opath 8@OCM; is a disorder #arge# affecting cardiac ! oc tes. It is characterised b %ne&p#ained 9entric%#ar h pertroph and histo#ogica# e9idence of ! ofibri##ar disarra . With respect to the !o#ec%#ar genetic basis of @OCM+ "hich of the fo##o"ing state!ents is tr%e$ a. b. c. d. e. A genetic abnor!a#it can be inherited in the absence of 9entric%#ar h pertroph Missense !%tations that res%#t in an a!ino acid "ith a change in charge appear to be associated "ith a !ore benign prognosis. On# candidate genes encoding ! osin proteins ha9e been associated "ith fa!i#ia# @OCM. 6atients "itho%t e&tensi9e ! ocardia# h pertroph or aortic o%tf#o" obstr%ction ha9e a benign prognosis. ,he prognosis is si!i#ar irrespecti9e of the !%tation #ocation in the 6 ! osin hea9 chain gene.

2). A /< o !an "ith 1no"n I@D presents "ith h pertension. @e has been getting infre7%ent angina and is c%rrent# on ateno#o# <( !g dai# . -e&t best treat!ent$ a. b. c. d. e. thiaKide i!d%r ena#apri# praKosin di#tiaKe!

2?. )< o !an "ith histor of CVA in past no" on "arfarin for AE. I-R %s%a## stab#e b%t no" presents "ith !e#aena and I-R H:. ,he coGad!inistered !edication !ost #i1e# to ca%se this isL a. b. c. d. e. phen toin ena#apri# er thro! cin proprano#o# 9erapa!i#

2:. /< o o#d pi#ot %ndergoes ro%tine ann%a# ph sica# e&a!ination and M3S,. ,he 3S, sho"s 1.< !! %ps#oping S, depression #atera## in the absence of pain. An e&erciseGtha##i%! is sho"n . there are re9ersib#e perf%sion defection in the anterior+ #atera# and apica# regions. ,he diagnosis is$ a. b. c. d. e. f. fa#se positi9e stress test 29 CAD e9idence of anterior ischae!ia o#d posterior infarct @OCM tric%spid 9a#9e disease

2B. A /( o !arathon r%nner co!p#ains of an occasiona# irreg%#ar heartbeat. A 1* #ead 3C4 is nor!a#. A ho#ter strip is sho"n+ de!onstrating "enc1ebach. ,he !ost appropriate !gt is$ a. b. c. d. e. I0O 66M angiograph reass%rance stress 3C4 stress tha##i%!

/(. A ** o fe!a#e presents "ith SO>. She has a >MI of 2( 81<(A of predicted;+ a histor of rhe%!atic fe9er+ and a c#eft pa#ate. ,he fo##o"ing cardiac res%#ts "ere obtainedL O* sats SVC ?1A IVC ??A RA ?)A RV ?BA fe!ora# arter B?A =o% "o%#d5 a. b. c. d. e. c#ose the sin%s 9enos%s ASD correct the VSD gi9e di%retics enco%rage "eight #oss gi9e penici##in proph #a&is

/1. A 1/ o bo presents "ith a s sto#ic !%r!%r "ith nor!a# sp#itting of S1 and S* d%ring inspiration. It is pans sto#ic and #o%dest at the LS3. ,he !%r!%r beco!es softer "it 9a#sa#9a !anoe%9re. CFR nor!a#+ MV6-3. M%r!%r has been present since age *. ,he ca%se is$ a. b. c. d. e. MV6 @OCM VSD ASD congenita# aortic stenosis

/*. An e#der# !an "ith 1no"n aortic stenosis has no" beco!e s !pto!atic. 6ea1 grad // !!@g+ LV3E 2(A. >est !gt is$ a. b. c. d. antifai#%re !edications AVR ba##oon 9a#9%#op#ast heart transp#ant

/2. 2( o "o!an+ *nd tri!ester. @istor of !itra# stenosis+ no" in AE. S sto#ic and !idGdiasto#ic !%r!%rs heard. 3cho sho"s !i#d MR+ MV 9a#9e area (.) c! * "itho%t ca#cification+ f%sion at co!!is%re+ nonGred%ndant #eaf#et+ and a p#iab#e 9a#9e "ith !oderate# se9ere p%#!onar h pertension. >est !gt is5 a. b. c. d. e. open heart MV rep#ace!ent ba##oon 9a#9%#op#ast !edica# therap ter!ination open MV 9a#9%#op#ast

//. 3#der# !an "ith past histor of AMI and recent# Ginserted VVD pace!a1er presents "ith pa#pitations. An 3C4 is sho"n . broad co!p#e&+ negati9e concordance+ dissociated p "a9es at a rate of 2((0!in+ irreg%#ar# irreg%#ar rate )( . 1(( "ith no pacing spi1es. Diagnosis is0 a. b. c. d. e. f. /<. be5 a. b. c. d. e. f. g. pace!a1erGind%ced tach cardia V, AE Af#%tter AIVR reGentrant tach cardia ?( o !an "ith a histor of ,IA+ h pertension and no other ris1s for I@D presents "ith AE. best !gt "o%#d "arfarin "ith I-R * G 2 "arfarin "ith I-R 1.< . 1.: "arfarin "ith I-R 1.< . *.< aspirin a#one heparin digo&in persantin

/). An e#der# "o!an "ho has h pertension+ AE+ CCE and arthra#gia presents "ith na%sea and 9o!iting. Medications inc#%de digo&in+ fr%se!ide+ s#o" C. Recent# co!!enced on ena#apri# and -SAID. >6 12(0:(+ @R 1((. Creat has gone fro! (.1/ to (.**. Digo&in #e9e# *.:. >est !gt$ a. b. c. d. e. f. stop digo&in and ena#apri# and chec1 digo&in #e9e# in *0? decrease digo&in dose and chec1 digo&in #e9e# in )0? stop digo&in+ ena#apri# and #asi& stop digo&in+ ena#apri#+ #asi& and -SAID and chec1 digo&in #e9e# in */ ho%rs stop digo&in ha#9e digo&in and stop -SAID

/?. A diabetic+ h pertensi9e !a#e "ith I@D and fre7%ent angina is referred for !anage!ent of his h pertension. @e is on ateno#o# <( !g dai# and has >6 1))0B: and @R )/. -e&t dr%g to add$ a. b. c. AC3 inhibitor i!d%r di#tiaKe!

d. e.

praKosin bendrof#%aKide

/:. )< o !a#e presents in p%#!onar oede!a. C%rrent R& is digo&in and a di%retic. 3cho sho"s LV h pertroph and di#atation "ith s sto#ic f%nction and a pea1 aortic gradient of /2 !!@g+ "ith a !ean gradient of 2( !!@g. >est therap is$ a. b. c. d. e. /B. a. b. c. d. e. AVR AC3 inhibitor ba##oon 9a#9%#op#ast nitrates transp#ant With regard to ser%! !ar1ers of ! ocardia# inI%r + "hich of the fo##o"ing is tr%e$ ,nI and ,nC reg%#ate the ca#ci%!Gindependent interactions bet"een actin and ! osin CCGMb is e#e9ated in <A of patients / ho%rs after onset of s !pto!s in AMI LD@ re!ains e#e9ated for the #ongest d%ration after MI ,-E #e9e#s indicate siKe of infarct ,n, #e9e#s are nonGspecific fo##o"ing rhabdo! o# sis

<(. A ?: o !an is ad!itted "ith p%r%#ent sp%t%!+ chest pain and SO>. CFR sho"s LLL pne%!onia. CC rises to :<( on da *+ and ,n, at da s / N ) is '(.(* 8-R '(.(*;. ,he SO> i!pro9es "ith antibiotics and fr%se!ide. @e contin%es to co!p#ain of chest pain+ re#ie9ed b !orphine. ,here are no ischae!ic changes on his 3C4. Repeat ,n, on da s : and 1( are (.(2. Which is the !ost #i1e# diagnosis$ a. b. c. d. e. AMI Dress#er s ndro!e UA6 63 3!p e!a

<1. A </ o h pertensi9e presents "ith se9er chest pain. @e is s"eat and pa#e. >6 1:(01((. ,here is a *0) !%r!%r of AI. ,he CFR is nor!a#. 3C4 sho"s 1 !! S, e#e9ation in V* . V/. >est initia# !anage!ent$ a. b. c. d. e. <*. a. b. c. d. e. i9 nitrates and heparin ,,3 thro!bo# sis %rgent angiogra! !orphine and !onitor reg%#ar 1* #ead 3C4s A CCU patient de9e#ops VE. =o% are ca##ed to r%n the res%s. Which of the fo##o"ing is incorrect$ ,he chances of s%ccessf%# defibri##ation dec#ine b appro& * . ?A for each !in%te the patient re!ains in cardiac arrest ,he A>Cs of basic #ife s%pport s#o" the rate of dep#etion of ! ocardia# high energ phosphate stores O9era## s%r9i9a# in hospita# after C6R a9erages 1/A Cardiac fi##ing d%ring C6R occ%rs passi9e# d%ring the %pstro1e of co!pression Eor"ard f#o" d%ring e&terna# cardiac co!pression is d%e to direct co!pression of the heart bet"een the stern%! and 9ertebra# bodies