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Acute myocardial ischaemia
Update 2011

Editor-in-Chief Dermot Phelan, Intensive Care Dept,
Mater Hospital/University College Dublin, Ireland
Deputy Editor-in-Chief Francesca Rubulotta, Imperial College, Charing
Cross Hospital, London, UK
Medical Copy-editor Charles Hinds, Barts and The London School of
Medicine and Dentistry
Self-assessment Author Hans Flaatten, Bergen, Norway
Editorial Manager Kathleen Brown, Triwords Limited, Tayport, UK
Business Manager Estelle Flament, ESICM, Brussels, Belgium
Chair of Education and Training
Committee
Marco Maggiorini, Zurich, Switzerland


PACT Editorial Board

Editor-in-Chief Dermot Phelan
Deputy Editor-in-Chief Francesca Rubulotta
Respiratory failure Anders Larsson
Cardiovascular critical care Jan Poelaert/Marco Maggiorini
Neuro-critical care and Emergency
medicine
Mauro Oddo
HSRO/TAHI Carl Waldmann
Obstetric critical care and
Environmental hazards
Janice Zimmerman
Infection/inflammation and Sepsis Johan Groeneveld
Kidney Injury and Metabolism.
Abdomen and nutrition
Charles Hinds
Peri-operative ICM/surgery and
imaging
Torsten Schrder
Education and Ethics Gavin Lavery
Education and assessment Lia Fluit
Consultant to the PACT Board Graham Ramsay

Copyright 2011. European Society of Intensive Care Medicine. All rights reserved.


Acute myocardial ischaemia
Learning objectives:

After studying this module on Acute myocardial ischaemia, you should be able to:

1. Recognise and risk stratify the patient with acute myocardial ischaemia
2. Undertake early management of acute myocardial ischaemia and manage
complications
3. Comprehend acute myocardial ischaemia and infarction
4. Give ongoing and discharge care (secondary prevention) and evaluate
outcome.


Contents


Contents
Introduction ................................................................................................................................................ 1
Terminology ............................................................................................................................................. 1
1. Recognition, immediate measures and risk stratification of the patient with acute myocardial
ischaemia .................................................................................................................................................... 4
Clinical features of ischaemic chest pain? .............................................................................................. 4
Risk stratification and triage ................................................................................................................... 5
Immediate management of ACS ............................................................................................................ 6
Ongoing physical examination ............................................................................................................... 8
Investigations ........................................................................................................................................ 10
Electrocardiography .......................................................................................................................... 10
Biochemical markers ......................................................................................................................... 15
Risk scoring systems .......................................................................................................................... 15
Echocardiography .............................................................................................................................. 18
Non-ST-segment elevation ACS ....................................................................................................... 20
2. Pathophysiology of acute myocardial ischaemia, infarction & cardiogenic shock ............................. 22
Understanding the underlying mechanisms ........................................................................................ 22
Understanding normal coronary artery anatomy ............................................................................ 24
Cardiogenic shock ............................................................................................................................. 24
3. Early specific management of AMI ...................................................................................................... 26
Acute management of STEMI .............................................................................................................. 26
Restoration of coronary patency ...................................................................................................... 26
Primary angioplasty in acute myocardial infarction ........................................................................ 28
Thrombolysis .................................................................................................................................... 30
Therapies used with reperfusion ...................................................................................................... 32
4. Management of complications ............................................................................................................. 38
Arrhythmia ........................................................................................................................................... 38
Post-infarction angina and infarct extension ...................................................................................... 38
Presentation ...................................................................................................................................... 38
Management ..................................................................................................................................... 39
Systemic embolisation .......................................................................................................................... 39
Haemodynamic instability ................................................................................................................... 39
Ventricular free wall rupture ................................................................................................................ 40
Presentation ...................................................................................................................................... 40
Management ...................................................................................................................................... 41
Ventricular septal rupture ..................................................................................................................... 41
Presentation ....................................................................................................................................... 41
Management ...................................................................................................................................... 41
Acute mitral regurgitation .................................................................................................................... 42
Presentation ...................................................................................................................................... 42
Management ..................................................................................................................................... 42
Right ventricular infarction .................................................................................................................. 43
Presentation ...................................................................................................................................... 43
Management ..................................................................................................................................... 44
Cardiogenic shock ..................................................................................................................................45
Presentation .......................................................................................................................................45
Diagnosis ........................................................................................................................................... 46
Initial management ........................................................................................................................... 46
Inotropic agents ................................................................................................................................. 47
Vasopressor agents ........................................................................................................................... 48
Managing patients with adequate tissue perfusion but pulmonary congestion .............................. 48
Revascularisation/further management in cardiogenic shock ........................................................ 49
5. How to give ongoing & discharge care (secondary prevention) and evaluate outcome ...................... 52
Secondary prevention ............................................................................................................................ 52
Aspirin ................................................................................................................................................ 52
Thienopyridines ................................................................................................................................. 52
Beta-blockers ..................................................................................................................................... 53
ACE inhibitors and angiotensin receptor blockers ........................................................................... 53
Lipid-lowering agents ........................................................................................................................ 55
Other anti-ischaemia agents .............................................................................................................. 55
Anti-arrhythmic therapy ....................................................................................................................56
Warfarin .............................................................................................................................................56
Contents
Lifestyle advice ................................................................................................................................... 57
Outcome of AMI ................................................................................................................................... 58
Conclusion .................................................................................................................................................59
Self-assessment ........................................................................................................................................ 60
PATIENT CHALLENGES ......................................................................................................................... 64


INTR

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Werns S. Acu
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asotti M, Pr
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pidly. The t
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optimal pat
ddition inte
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The eviden
rawn from
cy departm
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nd the asso
understood
erventions
larly useful
ute Coronar
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dustrialised
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ans should
ng ACS and
tions availa
nd accurate
tient care a
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nce for trea
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xclusion cri
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d when extr
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d society w
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th acute my
gy acute co
tients with
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d understan
d the range
able to inte
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and to min
e physician
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atment deci
re studies o
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iteria. The
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nt of unstabl
on (Part 1). T
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ise Textbook
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% of all
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ndrome (A
ocardial inf
at presenta
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se
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ocardial
uired to
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ACS is
s presentin
at have
m of
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its and risk
pulation. A
ial Infarctio
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25252538
le angina an
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5521556. P
k. 3rd editio
42 (Acute co
Introdu
is changing
ACS) has be
farction (A
ation to
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on. In:
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ng without
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occurs may
ent outcom
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ent settings
ns. Unstable
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ocardial inf
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esentation.
table.
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[20]
ACS
s with ACS
olytic thera
T wave inv
good sensit
symptoms
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NSTEMI) a
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rmine why
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ht also affect
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Yo
re
An
ht
An
Fi
ou can find
eferences.
ntman EM,
ACC/A
myoca
Cardi
Guide
of Pat
e822
ttp://www.a
nderson JL
ACC/A
angin
Colleg
Guide
availa
from:
940v1
itchett D, G
coron
1309
http:/
d out more

Anbe DT, A
AHA guidel
ardial infar
ology/Ame
elines (Com
tients with A
292. PMID
americanhe
L, Adams CD
AHA 2007
na/non ST-e
ge of Cardio
elines. Circu
able
http://circ.
1
Goodman S,
nary syndrom
1316. PMID
//www.cma
Task
e about acu
Armstrong P
lines for the
ction: a rep
rican Heart
mmittee to R
Acute Myoc
15339869
eart.org/pre
D, Antman E
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ology/Amer
ulation 200
.ahajournal
Langer A. N
mes: 1. Mat
D 11341143
aj.ca/cgi/rep
k 1. Recognitio
[21]
ute coronar
PW, Bates E
e managem
port of the A
t Associatio
Revise the 19
cardial Infar
esenter.jhtm
EM, Bridges
for the man
yocardial in
rican Heart
7; 116(7):e1
ls.org/cgi/re
New advanc
tching treat
. Full text a
print/164/9
on, immediate
ry syndrom
ER, Green L
ment of patie
American Co
n Task Forc
999 Guideli
rction). Circ
ml?identifie
s CR, Califf
nagement of
nfarction: a
Association
148304. PM
eprint/CIRC
ces in the m
ment to risk
vailable fro
9/1309.pdf
e measures an
mes in the f
LA, Hand M
ents with ST
ollege of
ce on Practi
nes for the
culation 200
er=3004542
RM, Casey
f patients w
report of th
n Task Force
MID 176796
CULATION
management
k. CMAJ 20
m
nd risk stratific

following
M, et al.
T-elevation
ice
Manageme
04; 110(9):
2
y DE Jr, et a
with unstabl
he American
ce on Practic
616. Full tex
NAHA.107.1
t of acute
001; 164(9):
cation


ent

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ccluding. A
ctivated pla
he GP IIb/I
ctivation. P
videnced b
avies MJ. T
83(3)
ibby P, Ther
2005;
ami S, Wille
segme
37(2)
idker PM, D
Rosuv
C-rea
18997
Task 2. Patho
HYSIOL
A, INFAR
ty of patien
ult from the
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and inhibi
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nt (pleiotro
mbus resu
Activated G
atelets, pro
IIIa recept
Platelet em
by elevated
The pathoph
: 361366.
roux P. Path
; 111(25): 34
erson JT. Co
ent-elevatio
: 141148. P
Danielson E
vastatin to p
ctive protei
7196
ophysiology of
LOGY O
RCTION
nts with acu
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pted, fissur
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troponin.
hysiology of
PMID 1067
hophysiolog
4813488. P
ontemporar
on myocard
PMID 2040
E, Fonseca F
prevent vas
in. N Engl J
f acute myocar
[22]
OF ACUT
N & CAR
ute MI hav
n of either
red or erod
erlying m
pment of c
ncreased LD
poproteins
ow HDL ch
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ownstream

f acute coro
77422
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ry treatmen
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01284
FA, Genest J
cular event
J Med 2008
rdial ischaemi
TE MYO
RDIOGE
ve coronary
totally or p
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mechan
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83262
nt of unstabl
on (Part 1). T
J, Gotto AM
s in men an
; 359(21): 2
a, infarction &
OCARDI
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y artery ath
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pid-lowerin
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let thromb
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omes. Heart
disease. Circ
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Tex Heart I
M Jr, Kastele
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21952207.
& cardiogenic
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heroma. A
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telets.
aques vuln
de collagen
ng agents m
so through
dom totally
n between
bi. Activatio
to thrombi
-infarction
t 2000;
culation
nd non-ST-
Inst J 2010;
ein JJ, et al
with elevate
PMID
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lesterol,
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Activation o
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myocardial
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Libby P, Fal
rable plaqu
sment strat
ew. PMID 14
of coagulati
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ctivation an
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es. Vessel v
esses have
medication
s?
rombus (pla
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egation (e.g
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is is usually
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coagulation
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of loss of m
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4530185
ion pathwa
activated p
nd the layi
so-called r
thrombus.
on by throm
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immediate
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bit cyclo-oxy
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ly consider
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orrelated
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able Angina
pply and d
thrombus d
cause). Art
plaque rupt
uction sp
n.
f acute myocar
[23]
ells SW, Lito
able patient
I). Circulati
ays by expo
platelets, le
ing down o
red thromb

mbus may
riction and
e relevance
kely to be
formation i
ygenases (e.
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comitant ad
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preserve m
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.
d with pre
al occlusio
to myocard
ue may be
a are usual
demand, wh
developing
terial inflam
ture.
pasm of an
rdial ischaemi
ovsky S, Rum
t: a call for n
ion 2003; 1
osed lipid
eads ultima
of fibrin clo
bus comple
y thus comp
spasm ma
e to treatm
useful in
is best limit
.g. aspirin),
el) or GPIIb
active ag
olytic agent
d cell throm
ministratio
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myocardial ti
therapies m
esses due to
Think of the
esenting s
on of a coro
dial damag
reduced by
lly caused
hich may b
g on a pre-
mmation o
n epicardial
a, infarction &
mberger J,
new definiti
08(14): 166
and fibrin
ately to
ot. Red cell
ex, which
plicate even
ay also pote
ent.
n the cont
ted by the u
ADP recep
/IIIa recept
gainst Re
s or anti-thr
mbus, but pa
n of anti-th
us lysis of re
issue.
may interrup
o platelet act
complicati
syndrome
onary arter
ge in its are
y timely re
by an imba
be due to o
existing pl
or infection
l artery or
& cardiogenic
et al. From
tions and ris
641672.

ls
en only mod
entiate
trol of W
use of antipl
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ed Throm
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pt these at
ctivation and
ions of such
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ry superim
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experiencin
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ny textbook
al presentati
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k followin
. In trials it
resent at ad
cases it is d
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c shock, 74.5
gurgitation,
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mbus. May
PCI.
nic
yocardial
delivery
ardiac trop
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ronary arte
and try to r
ion when
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dapted with p
nn Intern Me
ink to ESIC
hock: heart
Task 2. Patho
re, 3.4% isol
8% had oth
S, Boland J,
rum of card
ality. Result
tigators. Cir
S. Cardiogen
nding the pa
1585
siology
view the fol
shock. Work
diogenic sh
es that one m
spiral of ca
permission f
ed 1999; 131:
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t and vesse
ophysiology of
lated right v
er causes.
Sleeper LA
diogenic sho
ts of an Inte
rculation 19
nic shock co
aradigm. Ci
llowing diag
k through th
hock. Try an
might find.
rdiogenic s
from Hollenb
:4759. PMI
Conference
el dysfunct
Cardio
f acute myocar
[25]
ventricular
A, Porway M
ock and effe
ernational R
995; 91(3): 8
omplicating
irculation 20
gram and ar
he schema t
nd relate it t
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berg SM, Kav
ID 10391815
e: Elias Ilia
tion, summ
ogenic shock
remem
rdial ischaemi
shock, 1.7%
M, Brinker J,
ect of early r
Registry. SH
873881. P
acute myoc
003; 107(24
rticle relatin
to understa
o the clinica
vinsky CJ, an

adis, Camd
mer confere
k may comp
mber the vicio
a, infarction &
% tamponad
, Col J, et al
revasculariz
HOCK Regis
MID 78283
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4): 299830
ng to the pa
nd the inex
al findings a

nd Parrillo JE
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002. PMID
athogenesis
xorably prog
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E. Cardiogen
Cardiogeni
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cardial infar
f cardiogenic
shock
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ushner FG,
2009
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Data from th
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HINK Revie
escribe the t
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ed in perfor
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orbid illne
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Hand M, A
007 focused
agement of P
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Force on Pr
dian Cardio
ly Physician
te the ACC/
ST-Elevatio
ng Committ
Hand M, S
focused up
ST-Elevatio
2007 Focuse
utaneous Co
Focused Up
dation/Ame
elines. Circu
he TRANS
rombolysis
lity immed
is successf
f death, MI
pared to 17.
Fitchett D, B
ine early an
ction. N Eng
ew the hosp
treatment p
ke if you we
ts?
ce treatmen
tise of adm
et of sympt
for transfe
rming PCI
ss (particu
ry
c status.
Armstrong P
update of th
Patients wit
erican Colle
ractice Guid
ovascular So
ns: 2007 Wr
/AHA 2004
n Myocardi
tee. Circula
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n Myocardi
ed Update)
oronary Inte
pdate): a re
erican Hear
ulation 200
SFER-AMI
s for STEM
diately afte
ful or not.
, heart fail
.2% in pati

Borgundvaa
gioplasty af
gl J Med 20
pitals that re
patterns of t
ere admitted
[27]
nt choice a
mitting hos
toms
er to a card
I
ularly risk o
PW, Bates E
the ACC/AH
th ST-Eleva
ege of Cardi
delines: dev
ociety endor
riting Group
Guidelines
ial Infarctio
ation 2008;
, King SB II
C/AHA Guid
ial Infarctio
and ACC/A
ervention (u
eport of the
rt Associatio
9; 120(22):
study sugg
MI should b
er fibrinoly
This result
lure, severe
ients trans
ag B, Ducas
fter fibrinol
009; 360(26
efer to your
these linked
d urgently to
Task 3. Ea
and outcom
pital
diac cathete
of bleeding
ER, Green L
HA 2004 Gu
ation Myoca
iology/Ame
veloped in co
rsed by the
p to review
for the Ma
on, writing o
117(2): 296
II, Anderson
delines for m
on (updating
AHA/SCAI G
updating the
American C
on Task For
22712306
gest that hi
be consider
ysis withou
ted in a red
e recurrent
ferred only
J, Hefferna
lysis for acu
6): 270527
r hospital or
d hospitals?
o each one?
arly specific m
me:
erisation la
g and strok
LA, Halasyam
uidelines for
ardial Infarc
erican Heart
ollaboration
American A
new eviden
nagement o
on behalf of
6329. PMI
n JL, Antma
managemen
g the 2004
Guidelines o
e 2005 Guid
College of Ca
rce on Pract
6. PMID 199
igh-risk pa
red for tran
ut waiting t
duction in
t ischaemia
y for rescu
an M, Cohen
ute myocard
718. PMID 1
r that you re
? What treat
? Could you
management o
aboratory
ke)
mani LK, et
r the
ction: a
rt Associatio
n with the
Academy of
nce and
of Patients
f the 2004
D 18071078
an EM, et al
nt of patient
Guideline
on
deline and
ardiology
tice
923169
atients who
nsfer to a P
to see whet
the combi
a, or shock
ue PCI.
n EA, et al.
dial
19553646
efer to. Can
tment for A
suggest
f AMI

t
on
f
8
l.
ts
o
PCI-
ther
ined
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you
ACS

P
PC
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re
ac
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ho
gl

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th
pr
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R

Pr i mar y a
CI during t
Prim
Pharm
Rescu
he global t
oronary blo
rimary PCI
ower risk o
han thromb
equire tran
chieved wit
nitial succe
nfarction in
istal embol
ransient bu
arisch refle
RCA.
rimary per
oronary int
Grade 3) flo
hat PCI is s
hose >75 ye
DANAMI-2
wo hour wi
.3%), whils
e-infarction
chieved un
brinolysis
ospitals. Lo
lycoprotein
Recent meta
hrombolyti
romptness
f outcome,
which prima
ituations
Contr
Cardi
Sever
Haem

Revasculari
angi oplas
the early h
mary PCI
macoinvas
ue PCI afte
theme of ac
ood flow an
I can achie
f bleeding,
bolytic the
nsfer to a P
thin a 90-m
ess rates ex
n 2% to 4%
lisation of
ut severe hy
ex, which i
rcutaneous
tervention
ow in the in
superior to
ears, and th
study has
indow expe
st fewer pa
n, or disab
nprecedent
may well b
oading wit
n IIb/IIIa i
a-analyses
ic therapy.
s of percuta
and have
ary PCI is c
s in which
raindicatio
iogenic sho
re heart fai
modynamic
sation for c

sty i n acu
hours of ST
sive therap
er failed ph

cute STEM
nd overall
eve reperfu
, death, dis
rapy. This
CI-capable
minute per
xceed 90%.
% (a rate low
thrombus,
ypotension
s more com
s translumi
(PCI) incr
nfarct arter
o thromboly
hose with h
shown tha
erienced si
atients reac
ling stroke
ted inter-ho
be a better
th thienopy
inhibitors,
have sugg
Further an
aneous rep
identified
clearly sup
h PCI is cl
ons to thro
ock
ilure
cally signif
cardiogeni

[28]
ute myoca
TEMI can b
py (Pharma
harmacolog
MI is the rap
reduction
usion of the
sabling stro
holds true
e facility as
riod. In exp
. Complica
wer than fo
, ventricula
n associate
mmon with
inal corona
reases the r
ry, and sev
ysis for AM
haemodyn
at patients
ignificantly
ching the c
e (8% vs 13
ospital tran
reperfusio
yridines, w
may produ
gested that
nalyses hav
perfusion a
patient sub
perior (Lev
learly sup
ombolytic t
ficant vent
ic shock is
Task 3. Ea
ar di al i nf
be divided i
acologic pe
gic reperfu
pid restora
of ischaem
e infarct ve
oke, and re
e even if pa
s long as th
perienced
ations inclu
or thrombo
ar arrhythm
ed with the
h reperfusi
ary angiop
rates of res
veral rando
MI patients
namic and e
with STEM
y less clinic
combined c
3.7%). It sh
nsfer times
on strategy
with or with
uce even b
PCI is pre
ve identifie
as a key det
bpopulatio
vel 1 Eviden
perior to
therapy
tricular arr
discussed
arly specific m
far cti on
into
erfusion fol
usion.
ation of
mic time.
essel with
e-infarction
atients
his can be
hands,
ude re-
olysis),
mias and
Bezold
ion of the
plasty or pe
storation o
omised tria
s at higher
electrical i
MI treated
cal re-infar
clinical end
hould be no
s, and imm
y in many c
hout use of
etter vesse
ferable to
ed
terminant
ons in
nce).
thrombo
hythmias.
on page 49
management o

llowed by P
n
ercutaneou
of normal (
als have sug
risk, inclu
instability.
with PCI w
rction (1.6%
dpoint of d
oted that th
mediate
community
f adjuvant
el patency r

olysis

9.
P
trea
choice
STEM
be
w
minutes
unlik
thro
s
adm
w
PCI i
superior
f AMI
PCI)
us
(TIMI
ggested
uding
The
within a
% vs
death,
his trial
y
rates.
PCI is the
atment of
e in acute
MI if it can
achieved
within 90
s. If this is
kely, then
ombolysis
should be
ministered
within 30
minutes
is clearly
r in some
groups

Si

C
Pr
by
of
to
In
th

O
R
th
pr
m
in
w
An
H
Ke
St
M

Q
m

A.
re

ituations
Elder
Large
Prior
High
Coronary
rimary PCI
y the risk o
f the infarc
o be superi
n ST elevat
hat primary
Other indi
Rescue PCI
herapy, alth
rimary ang
mortality is
n the comb
with rescue
ndersen HR
al. A c
myoca
12930
Hochman JS
Early
cardio
revasc
1999;
eeley EC, B
throm
review
12517
tone GW, G
of ang
myoca
11919
Montalescot
Platel
myoca
11419
Q. What te
maintain v
. Balloon an
etracts with
s in which
rly patients
e anterior i
r myocardi
h bleeding r
stenting f
I for AMI r
of abrupt v
ct-related a
or to ballo
tion myoca
y stenting
ications f
is indicate
hough the
gioplasty, r
higher. Lim
bined endp
PCI.
R, Nielsen T
comparison
ardial infar
0925
S, Sleeper LA
revasculari
ogenic shoc
cularize occ
341(9): 625
oura JA, Gr
mbolytic the
w of 23 rand
7460
Grines CL, C
gioplasty wi
ardial infar
304
G, Barragan
let glycopro
ardial infar
426
echniques
vessel pat
ngioplasty p
a conseque
h PCI may
s (age >75
infarction
al infarctio
risk.
for acute
results in a
vessel closu
artery and
on angiopl
ardial infar
was superi
for angiop
ed for patie
initial succ
reocclusion
mited avai
oints of de
TT, Rasmuss
n of coronary
ction. N En
A, Webb JG
ization in ac
ck. SHOCK I
cluded coron
5634. PMI
rines CL. Pr
erapy for acu
domised tri
ox DA, Gar
ith stenting
ction. N En
n P, Wittenb
otein IIb/III
ction. N En
s of angio
tency?
produces cir
ent reductio
[29]
y be prefe
years)

on or prior
e myocard
a significan
ure, recurre
restenosis
lasty for th
rction, how
ior to prim
plasty in A
ents who fa
cess rate is
n is more c
ilable data
eath or hea
sen K, Thue
ry angioplas
ngl J Med 20
G, Sanborn T
cute myocar
Investigator
naries for c
ID 1046081
rimary angi
ute myocard
als. Lancet
rcia E, Tchen
g, with or wi
ngl J Med 20
berg O, Eco
Ia inhibition
ngl J Med 20
oplasty m
rcumferenti
on in stenos
Task 3. Ea
erable to
r coronary
dial infarc
nt reductio
ent in-hosp
. Coronary
hese outcom
wever, early
mary balloo
AMI
ail thrombo
s lower tha
common, a
suggests a
art failure a
esen L, Kelb
sty with fibr
003; 349(8)
TA, White H
rdial infarct
rs. Should w
ardiogenic
13
oplasty vers
dial infarcti
2003; 361(
ng JE, Griff
ithout abcix
002; 346(13
ollan P, Elha
n with coron
001; 344(25
may be use
ial and long
is. Antiplat
arly specific m
thrombo
artery byp
ction
n in morta
pital ischae
y stenting h
mes when d
y trials did
on angiopla
olytic
an that of
nd
a reduction
at 30 days
baek H, Tha
rinolytic the
): 733742.
HD, Talley J
tion compli
we emergen
shock? N E
sus intraven
ion: a quant
9351): 132
fin JJ, et al.
ximab, in ac
3): 957966
adad S, Villa
nary stentin
5): 189519
ed to indu
gitudinal spl
elet agents
management o
olysis
pass graftin
ality but is
emia, reoc
has been sh
done elect
d not demon
asty.
n

ayssen P, et
erapy in acu
. PMID
JD, et al.
icated by
ntly
Engl J Med
nous
titative
20. PMID
Compariso
cute
6. PMID
ain P, et al.
ng for acute
903. PMID
uce and
lits in plaqu
are adminis
PC
consider
throm
f AMI
ng
limited
clusion
hown
ively.
nstrate


ute
on

e
ue that
stered
CI can be
red after
failed
mbolysis

to
pr
ef
re
(b
wh
as

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as

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re

Ar

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su

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liv
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ca

Q

A.
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m
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de
or

G

o decrease fu
rocedure. T
ffective trea
eduction in
brachythera
which elute s
ssociated wi
Thr ombol
hrombolyt
epartment
iven within
A goal is d
ssociated w
Mortality-
eduction ap
rmstrong P
the fu
12777
Q. How do
urvival?
. Administe
ves per 100
atients pres
ase basis. M
Q. What is
. The 30-da
55 years of
igher risk of
mortality me
he benefit o
emonstrated
r of complic
ottlieb S, Be
mana
acute
17208
urther throm
he placeme
atment for c
restenosis,
apy) has bee
small amoun
ith significa
lysi s
tic therapy
t. Initial rep
n two hour
door to ne
with excess
- Relative r
pproximat
W, Collen D
uture is here
7317
oes the tim
ered within
0 patients t
senting beyo
Maximal ben
s the effec
ay mortality
age, to 25%
f thromboly
eans that thi
of thromboly
d in trials. S
cations from
ehar S, Hod
agement, ho
myocardial
8084

mbus forma
ent of stents
atheter-ind
restenosis s
en used to tr
nts of anti-i
ant increase
should be
perfusion i
s of sympt
eedle tim
s mortality
reduction in
ely 2%, or
D, Antman E
e and now. C
me from s
06 hours o
treated; with
ond 12 hour
nefit is seen
ct of age u
y of non-thro
% for patient
ysis complic
is group has
ysis in patie
Some would
m thromboly
d H, Zahger
ospital and l
l infarction.
[30]
ation. Late r
s allows a la
duced dissec
still remain
reat stent ob
inflammato
es in stent p
e given as e
is expected
tom onset.
me of less
y.
n death rat
20 deaths
E. Fibrinoly
Circulation
symptom
of onset, fib
hin 712 ho
rs may be co
if administ
upon outc
ombolysed
ts >75 years
cations than
s the highes
ents >75 yea
d recommen
ysis in this g
r D, Leor J, H
long-term o
. Am J Med
Task 3. Ea
restenosis i
arger lumen
ction. While
s problema
bstruction.
ory material
atency in hi
early as pos
d in approx

than 30 m
te at 35 da
per 1000 p
ysis for acut
2003; 107(
m onset to
brinolytic th
ours, 20 live
onsidered fo
ered within
come foll
AMI patien
s of age. Pat
n younger p
st absolute b
ars of age h
nd PCI for p
group.
Hasdai D, e
outcomes of
d 2007; 120(
arly specific m
s a major lim
to be obtain
e stents prod
tic. Radiatio
Drug-Eluti
ls such as si
igh-risk pat
ssible in th
ximately 80
minutes.
ys of about
patients tre
te myocardi
(20): 2533
o treatmen
herapy saves
es per 1000
or thrombo
n 60 minute
lowing th
nts ranges fr
tients aged >
atients, but
benefit from
as been less
patients at h
et al. Trends
f elderly pat
(1): 9097.
management o
imitation of
ined and is a
duce a sign
on treatmen
ing Stents (
irolimus hav
tients.
he emergen
0% of patie
Delay is
ut 21% (abs
reated).
ial infarctio
2537. PMID
nt influen
s approxim
patients tre
olysis on a ca
es of onset.
hromboly
rom 5% in p
>60 years h
t high basel
m thromboly
s well
high risk of
s in
tients with
PMID
f AMI
f this
also an
ificant
nt
(DES),
ve been
ncy
ents if
olute

n:
D
nce
mately 30
eated.
ase-by-
ysis?
patients
have a
ine
ysis.
death



Th

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ag

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be

B
ou
or

hromboly
irst genera
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omplicatio
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econd-gen
tPA), a natu
recombinan
treptokinas
accelerated
he GUSTO
mortality in
000 patien
aemorrhag
gents are u
he GUSTO I
throm
1993;
he GUSTO A
activa
functi
1993;
annon CP, G
al. TN
altepl
Throm
Circul
llis K, Brene
but ea
PMID
urther bioe
equire weig
njection. Th
ncreased fib
t-PA, morta
minutes apa
Contraind
elow
enefit is co
utcomes ar
r with facil
ytic agen
ation throm
ng plasmin
n, intracra
s is rare bu
eration age
urally occu
nt tissue-ty
se and acts
d regimens
trial 30-da
n the SK gro
nts treated.
ge, particul
used.
Investigato
mbolytic stra
329(10): 67
Angiograph
ator, strepto
ion, and sur
329(22): 16
Gibson CM,
NK-tissue pl
lase in acute
mbolysis in
lation. 1998
er S. New fi
asier to adm
D 14740966
engineerin
ght-based d
his allows f
brin specif
ality is not
art; Tenect
dications (
onfined to A
re achieved
litated PCI

nts (Fibrin
mbolytic ag
n and are co
anial haem
ut can be tr
ents were e
urring subs
ype plasmi
s more dire
s of tPA pr
ay mortalit
oup (7.4%)
. These age
larly in pat
rs. An inter
ategies for a
73682. PM
hic Investiga
okinase, or b
rvival after
6151622. P
, McCabe CH
lasminogen
e myocardia
Myocardial
8; 98(25): 2
ibrinolytic a
minister. Cle

ng of rt-PA
dosing, an
for simplif
ficity and im
t impacted.
teplase (TN
(absolute
ACS with S
d if routine
.

[31]
nolytic ag
gents such
onsidered
morrhage, o
roublesome
engineered
stance prod
inogen act
ectly at the
oduce bett
ty in the tP
), saving an
ents have s
tients olde
rnational ra
acute myoca
MID 820412
ators. The e
both on cor
acute myoc
PMID 8232
H, Adgey A
n activator c
al infarction
l Infarction
28052814.
agents for M
eve Clin J M
has produ
d have lon
fication of
mproved 9
. Reteplase
NK-tPA), is
e and rela
ST-segmen
ely adminis
Task 3. Ea
gents)
as streptok
non-speci
ccurs in ab
e.
d from tiss
duced by e
ivator, rt-P
e fibrin sur
ter vessel p
PA group (6
n estimate
slightly hig
r than 75 a
ndomized t
ardial infarc
23
effects of tis
ronary-arter
cardial infar
2430
AA, Schweig
ompared w
n: results of
n (TIMI) 10B
PMID 986
MI: as effect
Med 2004; 7
uced newer
nger half-liv
drug admi
90-minute
e (r-PA) is
s given as a
ative) to t
nt elevation
stered to p
arly specific m
kinase indu
ific. The m
bout 0.6%
ue plasmin
endothelium
PA) is less a
face. Weig
patency rat
6.3%) was
d ten addit
her risk of
and when G
trial compar
ction. N Eng
sue plasmin
ry patency, v
rction. N En
er MJ, Sequ
with front-lo
f the TIMI 1
B Investigat
0780
ive as curre
71(1): 20, 23
r agents tha
ves, allowin
nistration.
patency ra
given in tw
a single bol
thrombol
n or new LB
patients wit
management o
uce a lytic
most devast
of patients
nogen activ
m. Alteplas
antigenic t
ght-adjuste
tes than SK
14% lower
tional lives
f intracrani
GP IIb/IIIa
ring four
ngl J Med
nogen
ventricular
ngl J Med
ueira RF, et
oaded
10B trial.
tors.
ent agents,
325, 2930
at may not
ng for bolu
. Despite
ates compa
wo boluses
lus.
lysis see
LBBB. Wors
th UA, NST
f AMI
state
tating
s.
vator
se
than
ed,
K. In
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ial
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ared to
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lip
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AB
Previous ha
stroke
Other strok
cerebrovas
months
Intracrania
Active inte
weeks (men
Aortic diss
suspected
Do
dvice if relat
Ther api es
Q. Why ar
ome com
. Approxim
ollowing thr
trands of re
ndeed may b
Underlying u
pid stabilisi
ncrease the c
angiotension
wall stresses,
SOLUTE
aemorrhag
ke or
scular accid
al neoplasm
rnal bleedi
nses exclud
ection, kno
not forget t
tive contrai
s used wit
e additio
monly us
ately 50% o
rombolysis.
ed thrombus
be pro-thro
unstable pl
ing agents. S
chance of b
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th r eper fu
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sed agent
of patients f
Current pla
s. They hav
ombotic, req
aque may b
Such therap
leeding. Oth
ng enzyme) i
ng-term ben
[32]
(Advisory
Severe hype
controlled a
Oral antico
known blee
Recent maj
ncluding h
Previous all
Traumatic C
Active pept
Pregnancy
Recent stre
risk of alle
effectivenes
History of p
pathology n
Chronic hyp
e contraindi
present and
fusi on
apies nece
ts?
fail to attain
asminogen
ve little effe
quiring con
be pacified
pies may sta
her therapi
inhibitors m
neficial effec
Task 3. Ea
REL
y following
ertension (
after sedat
agulation t
eding diath
jor trauma
head traum
lergic reac
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tic ulcer dis
eptokinase.
ergy, antibo
ss)
prior CVA
not covered
pertension
ications for
d uncertain
essary aft
n or sustain
activators (
ct on under
ncomitant h
by antiplat
abilise throm
es such as
may decreas
cts.
arly specific m
LATIVE
clinical co
(180/110
ion and an
therapy (IN
hesis
, surgery (
ma
tion to dru
sease
. Use differ
odies may r
or intracer
d in contra
n
thrombolys
, or conside
ter AMI?
coronary ar
thrombolyt
rlying expos
eparin (anti
telet agents
mbus or ves
-blockers a
se myocardi
management o
onsideratio
mmHg) no
nalgesia
NR >2.5);
4 weeks)
ug to be use
rent agent
reduce
rebral
aindication
sis. Seek sp
er urgent PC
What are
rtery patenc
ytics) destro
sed thrombi
ti-thrombin
and possib
ssel walls bu
and ACE
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f AMI
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ed

ns
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CI.
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cy
oy fibrin
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al; CLARITY
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R, Berger PB
tigators. Ea
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enez-Silva J
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21): 22182
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[35]
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HORIZONS
ment with
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that has be
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c): gold stan
ents referre
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in
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TEMI patie
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dek D, et al
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329(10): 67
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2027. PMI
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They may h
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, and ACE)
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out contrai
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) should be
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Task 3. Ea
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ment
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schaemia a
pirin
roglycerin
parin
lockade, an
underlying
agnostic cor
cclusion of
er coronar
a cannot b
mic instab
as its dual
terload) wi
tion angina
if the culpr
patency ma
rtery bypas
with left m
table for P
row DA. Ma
elines Summ
nwald E, Zip
ovascular M
978141604
c emboli
in therapy
ynamic
patients wi
cal complic
useful techn
ng table de
graphy in d
n any patie
d at:
and residua
(usually i.v
nd conside

stenosis
ronary ang
f the infarc
ry territorie
e controlle
bility, an in
effect (of i
ill be expec
a is an indi
rit lesion is
ay not be as
ss grafting
main diseas
CI.
anagement
mary ACC
pes DP, Libb
Medicine. 8t
41030. pp. 1
isation
section in
instabil
th haemod
cations mu
nique to di

emonstrate
differential
ent with sh
[39]
al thrombu
v.)
eration of c
giography s
ct artery an
es.
ed medical
ntra-aortic
improving
cted to be b
ication for
s suitable, r
s good as th
(CABG) sh
se, three-v
of Chronic
C/AHA Card
by P, editor
th ed. Phila
14051417
Task 5.
lity
dynamic de
ust be cons
iagnose thi
es the use o
l diagnosis
hock follow
Task
us
calcium-ch
should be p
nd to evalu
lly or is acc
balloon pu
coronary p
beneficial.
revascular
recognising
hose with e
hould be co
vessel disea
Ischemic H
diology Guid
rs. Heart Di
delphia: Els

ecompensa
idered. Ech
is group of
of right hea
of complic
wing myoca
4. Manageme
hannel bloc
performed
ate signific
companied
ump (IABP
perfusion p

risation. PC
g that acut
elective an
onsidered
ase, and
Heart Diseas
deline Summ
isease: A Te
sevier Saun
ation after
hocardiogr
conditions
art cathete
cated AMI
rdial infarc
ent of complica
ckers.
d to exclude
cant lesion
d by
P) should b
pressure an
CI can be
te outcome
ngioplasty.

se: AHA/AC
maries. In:
extbook of
nders; 2007
AMI, a nu
raphy can b
s (see table
erisation an
. Consider
rction.
Rea
indica
ations
e
ns in
be
nd
es and


CC

.
umber
be an
e
nd
these
ad about
tions for
CABG
Task 4. Management of complications
[40]


Use of right heart catheterisation and echocardiography in diagnosis

DIAGNOSIS CVP PAOP CO OTHER
FINDINGS ON
PAC
ECHOCARDIOGRAPHY
Mechani cal
compli cati ons





Free wall
rupture

Usually
tamponade
physiology. RA
mean, RV and
PA end-
diastolic, and
PAOP pressures
are elevated and
within 5 mmHg
of one another
Pericardial effusion
with tamponade and RV
diastolic collapse; may
visualise
pseudoaneurysm
Acute
ventricular
septal defect

Left-to-right
shunt with
oxygen step-up
at RV level; V
waves may be
seen in PAOP
tracing
Visualisation of left-to-
right shunting with
colour Doppler; can
sometimes visualise
defect as well
Acute mitral
regurgitation

V waves in
PAOP tracing
Regurgitant jet
apparent on colour
Doppler; can diagnose
papillary muscle
rupture with flail leaflet
RV i nfar cti on

or
normal


RV dysfunction
Pump fai lure
(car di ogeni c
shock)

Decreased overall LV
performance; regional
wall motion
abnormalities;
dyskinetic or
aneurysmal segments
may be seen
CVP = central venous pressure; PAOP = pulmonary artery occlusion pressure; CO = cardiac
output; PAC = pulmonary artery catheterisation; RV = right ventricular; RA = right atrial; PA =
pulmonary artery

Ventricular free wall rupture

Presentati on

Ventricular free wall rupture typically occurs with a bimodal distribution during
the first week after infarction, with one peak around 24 hours and a second peak
at 35 days. Free wall rupture presents as a catastrophic event with shock and
electromechanical dissociation.



Th
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th
af
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he classic p
with a first i
he incidenc
fter infarct
Managem
alvage of p
ericardio-c
eart cathet
atheterisat
later J, Brow
shock
myoca
emerg
Coll C
Ventricu
Presentati
he inciden
020 fold i
entricular s
ardiogenic
hrill. The h
step-up in
ulmonary a
istinguish v
ecause bot
VSR, they re
iagnosis is
Use of right
bove).
Managem
Operative re
eptal ruptu
hould be tr
efect can ra
herapy with
itroprussid
iming of su
perative re
lacement o
elected pat
patient is a
infarction.
ce of cardia
tion may ac
ment
patients wit
centesis, an
terisation c
tion and ec
wn RJ, Anto
k due to card
ardial infar
gently revas
Cardiol 200
ular sept
i on
nce of ventr
in the thro
septal rupt
shock, wit
hallmark fin
n SvO
2
from
artery cath
ventricular
th can prod
esult from
most easil
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ment
epair is the
ure may occ
reated very
apidly enla
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de), when t
urgery has
epair shoul
of a percuta
tients.
an elderly f
Early repe
ac rupture,
ctually incr

th free wal
nd surgical
can help m
chocardiogr
onelli TA, M
diac free-wa
ction: a rep
scularize oc
0: 36(3 Sup
tal ruptu
ricular sept
ombolysis e
ture presen
th a pansys
nding is a l
m right atri
heter tracin
r septal rup
duce drama
increased
ly made wi
heterisatio
e only viabl
cur prior to
y aggressive
arge and re
soactive ag
tolerated, c
been cont
ld be under
aneous sep
[41]
female with
erfusion vi
, but throm
rease that
ll rupture i
l repair. Em
make the dia
raphy abo
Menon V, Bo
all rupture o
port from th
ccluded coro
ppl A): 1117
ure
tal rupture
era. Patien
nt with sev
stolic murm
left-to-righ
ium to righ
ng, it can b
pture from
atic v wav
pulmonary
ith echocar
on and echo
le option f
o haemody
vely with su
esult in hae
gents and a
can be help
troversial, b
rtaken earl
ptal occlud
Task
h chronic h
a PCI or th
mbolytics g
risk.
s possible
mergent ec
agnosis (se
ove).
oland J, Col
or tampona
he SHOCK T
onaries for c
1122. PMI
e (VSR) ha
ts who hav
vere heart f
mur and pa
ht intracard
ht ventricle
be difficult
m mitral reg
ves (in the
y vein flow
rdiography
ocardiogra
for long-ter
ynamic com
urgical mea
emodynam
afterload r
pful but sh
but most a
ly, within 4
ding device
4. Manageme
hypertensi
hrombolyti
given later t
with prom
chocardiog
ee table Us
l J, et al. Ca
ade after acu
Trial Registr
cardiogenic
D 10985714
s decrease
ve
failure or
arasternal
diac shunt
e). On
to
gurgitation
case of
w). The
y (see table
aphy
rm surviva
mpromise.
ans bearing
mic collapse
educers (su
ould not d
authorities
48 hours o
may be co
ent of complica
ion, presen
ic therapy
than 14 ho
mpt recogni
graphy or r
se of right
ardiogenic
ute
ry. Should w
c shock? J A
4
ed


n,
e
al. Occasion
. These pat
g in mind t
e. Medical
uch as sod
delay surge
now sugge
of the ruptu
ontemplate
Revie
know
PAC wa
t
ations
nting
reduces
ours
ition,
right
heart

we
Am
nally, a
tients
that the

dium
ry.
est that
ure.
ed in

ew your
wledge of
aveform
tracings

H
M
Bi
M

A

P

Pa
is
ap
to
bl
R

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pu
m
ea
ve
es

E
in
pu
ca
M

Te

D
sh
de

Hinds CJ, W
Ltd; 2
Menon V, We
and p
myoca
we em
Am C
irnbaum Y,
acute
PMID
Murday A. O
89(12
Acute mi
Presentati
apillary mu
s rarely hae
pical mur
o ischaemia
lood suppl
RCA).
Papillary m
ulmonary o
muscle rupt
arly systole
entricle. M
specially w
chocardiog
ncludes fre
ump failur
atheterisat
Managem
emporising
Afte
Intr
Ino
inad
Definitive th
hould be un
eterioratio
atson JD. In
2008. ISBN
ebb JG, Hil
profile of ven
ardial infar
mergently re
Coll Cardiol
Fishbein M
myocardial
D 12409546
ptimal man
2): 1462146
itral reg
i on
uscle dysfu
emodynam
rmur of m
a or infarct
y (usually
muscle ru
oedema, h
tures, the m
e because o
More impor
when cardia
graphy is e
e wall rupt
re. Haemod
tion may al
ment
g measure
erload redu
ra-aortic ba
tropes or v
dequate.
herapy is su
ndertaken
on can be su
ntensive Ca
N: 978-0-702
lis LD, Slee
ntricular sep
ction: a rep
evascularize
2000; 36(3
MC, Blanche
l infarction.

nagement of
66. PMID 14
gurgitati
unction is c
mically sign
mitral regur
tion of the
from the p
upture, on
ypotension
murmur of
of rapid eq
tantly, the
ac output is
extremely u
ture, ventr
dynamic m
lso be help

s include:
uction with
alloon cou
vasopresso
urgical val
as soon as
udden.
[42]
are: A Conci
20259-6-9.
eper LA, Abb
ptal rupture
port from th
e Occluded
3 Suppl A): 1
e C, Siegel R
. N Engl J M
f acute vent
4617565
ion
common a
nificant; the
rgitation is
posterior
posterior d
n the other
n, and card
f acute mitr
qualisation
e murmur
s low.
useful in th
ricular sept
monitoring
pful (see tab
h nitroprus
unterpulsat
ors if cardia
lve repair o
s possible,
Task
ise Textbook
pp. 11912
boud R, Dza
e with cardi
he SHOCK T
Coronaries
11101116. P
RJ. Ventricu
Med 2002; 3
tricular sept
fter inferio
e charact
s typically p
papillary m
escending
r hand, pre
diogenic sh
ral regurgi
of pressur
r may be s
he differen
tal rupture
with pulm
ble above).
sside
tion pump
ac output o
or replacem
since clini
4. Manageme
k. 3rd editio
3 (Vasodila
avik V, et al
iogenic shoc
Trial Registr
in cardioge
PMID 1098
ular septal ru
347(18): 142
tal rupture.
or myocard
eristic ho
present. It
muscle, wh
branch of
esents dr
hock. When
itation may
res in the le
soft or in
tial diagno
, and infar
monary arte
.
(IABP)
or blood pr
ment, which
cal
ent of complica
on. Saunder
ator therapy
l. Outcome
ck after
ry. SHould
enic shocK?
85713
rupture afte
261432.
Heart 200
dial infarct
olosystoli
t is commo
hich has a s
a dominan
ramatical
n a papillar
y be limite
eft atrium
naudible,
osis, which
rct extensio
ery
ressure is
ch
ther
as
sur
sh
ations

rs
y)
? J
r
3;
tion but
ic
only due
single
nt
lly with
ry
d to
and left
h
on with
Medical
apy may
ssist with
rgery but
hould not
delay it

Kh
Lu
M
Th


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in

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K
el
sp

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fin
ri
PA
de
he
w
fin

R
sh
in
be
fu
no
di
hy

han SS, Gra
PMID
ung B. Man
464. P
Marwick TH,
mech
19786
hompson C
Cardi
acute
SHou
shocK
10985
Right ven
Presentati
Right ventri
nfarction an
atients pre
Kussmauls
levation in
pecific).
Diagnosis is
ndings on
ght ventric
AOP and lo
emonstrate
elp differen
which may p
ndings.
Recent pape
hock has a
nfarction. H
etter long-
unction usu
ote that de
iuretics, as
ypotension
ay RJ. Valvu
D 1811874
nagement of
PMID 12639
, Lancellotti
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6708
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ogenic shoc
myocardial
uld we emer
K? J Am Col
5712
ntricula
i on
icular ischa
nd is clinic
esent with h
sign and c
right prec
s confirmed
right heart
cular end-d
ow cardiac
e depresse
ntiate righ
present wit
ers have sh
short-term
However, i
term progn
ually return
espite the e
s hypovolae
n.

ular emerge
f ischaemic
9884
i P, Pierard
d diagnosis.
E, Sleeper L
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ll Cardiol 20
ar infarc
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hypotensio
clear lung f
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diastolic pr
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[43]
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V
o

in
It is im
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to perf
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Not all
JVPs in
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ations

9

c
ferior
mportant
nk of this
gnosis as
specific
atment is
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lead
amination
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need for
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O
Ja
Pf

M

Th
th
in
flu

in
ve
an

In
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factors (h
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pp. 6476
more infor
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Hinds CJ, W
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myocardial
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a balance b
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nitial stabil
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Vasodilator
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agents
atson JD. In
2008. ISBN
active agents
with inade
ular suppor
ne, a selec
contractili
patients w
. Dobutam
hypovolae
pitate tachy
output, an
0 mmHg, b
e, a phosph
chanisms n
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rs (such as
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s)
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gestion rem
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on and ade
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rrhythmias
r that incre
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When arteri
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nd increase
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mortality in
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ine, a selec
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congestion
oration of
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therapy (w
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n has the po
aution in p
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tal Heart J 2
ts
e remains
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ective veno
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[48]
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patients wit
ts with low-
2003; 4(Sup
inadequat
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recent rand
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lytic therap
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pid-lower
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[56]
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routinely co
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value; how
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Cardiol 199
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i GG, Crea F
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[58]


Outcome of AMI

The in-hospital mortality from acute ST elevation MI has been steadily
decreasing over the past three decades from 1530% in the 1970s to
approximately 10% in 1980 and now to around 6% in the new millennium.
Despite improved mortality, 60% of all deaths occur within the first hour
(usually from VF), and usually before reaching a medical facility. Modern
management of acute MI has undoubtedly contributed to decreased mortality,
but further significant reduction in mortality must come from management
strategies within the first hour of the onset of symptoms.

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ement of AC
gthen clini
tean manif
ntaining kn
ations of m
unt of work
es not only
are, but an
reciation o
tinuing ski
schaemic h
ous countri
elow.
er=3003999
Concl
ndromes w
erventions
arge eviden
CS.
ical skills d
festations a
nowledge o
myocardial
kload for
y good clini
up to date
of the rapid
ills in the u
heart disea
ies. You ca
9
lusion
will
which
nce base
directed
and
of

ical
e
dly
use of
ase will
n find

Self-assessment
[60]

SELF-ASSESSMENT

SELF-ASSESSMENT QUESTIONS

EDIC-style Type K

1. ACS can be subdivided into:
A. Unstable angina
B. Unstable angina with ST-segment depression
C. Myocardial infarction with ST-segment elevation (STEMI)
D. Myocardial infarction without ST-segment depression (non-STEMI)

2. Medications useful to prevent and control white thrombus include:
A. Dalteparin
B. Cyclo-oxygenase activators
C. Aspirin
D. Inhibitors of ADP receptor-mediated platelet aggregation

3. A 73-year-old female patient with a previous history of STEMI is
transported to the hospital with signs and symptoms of ACS. In the
ambulance she is given oxygen through a face mask, she is given
nitroglycerin sublingual and after venous access is established, she is
also given morphine 2.5 mg i.v. What else should be considered for her in
the pre-hospital setting (by non-medical ambulance personnel)?
A. Intravenous glucose 50 mg/ml with insulin
B. Rapid infusion of Ringer Acetate
C. Aspirin 160 mg to be chewed
D. Paracetamol 250500 mg per os

4. Which of the following strategies is considered to be correct in
reopening the occluded coronary artery (PCI) of a patient with STEMI?
A. Fibrinolytic therapy in all patients followed by PCI in selected cases
B. Fibrinolytic therapy only if PCI is not possible to perform within the first 90
minutes
C. According to risk profile, patients with STEMI should be considered for
transfer to a PCI-capable centre
D. If fibrinolytic therapy is given one has to wait at least two hours before
conducting PCI

5. Regarding area of infarction, which are the correct statements
regarding the most appropriate ECG leads?
A. Inferior infarction is seen in II, III and aVF
B. Anterior infarction is seen in V5 and V6
C. True posterior infarction is characterised by a tall R wave in V1
D. Septal infarction is seen in I, aVL, V5 and V6

6. Regarding troponins as biomarkers for cardiac injury
A. Troponins are equal with CK regarding sensitivity
B. CK has a better specificity than troponins
C. Troponins are the first biomarker to rise after myocardial ischaemia
D. Troponins are elevated for more than 48 hours after myocardial injury

Self-assessment
[61]


7. Which of the following are complications of PCI?
A. Re-infarction in 810 %
B. Ventricular arrhythmias
C. Sudden hypertensive episodes (BezoldJarisch reflex)
D. Distal embolisation of thrombus

8. Clopidogrel:
A. Is an adenosine diphosphate-receptor antagonist
B. Inhibits activation and aggregation of platelets
C. Has similar actions to aspirin
D. Is usually given as a 3 to 6 g loading dose

9. Recognised complications after acute myocardial infarction include:
A. Free wall rupture
B. Atrial septal rupture
C. Acute mitral regurgitation
D. Cardiogenic shock

10. A 59-year-old male with STEMI suddenly develops hypotension on
day one after onset of symptoms. A diagnosis of cardiogenic shock is
established after introduction of a PA catheter. Regarding the further
management of this patient, which of the following should be
considered?
A. Immediate infusion of crystalloids until MAP stabilises above 90 mmHg
B. Active treatment of complicating arrhythmias or conduction defects
C. The use of dobutamine to raise CI towards 3 litre/min/m
2

D. Aggressive use of beta-blockers may prevent further instability


EDIC-style Type A

11. After acute myocardial infarction (AMI), PCI is clearly superior to
thrombolysis in all of the following EXCEPT
A. Cardiogenic shock
B. Severe heart failure
C. Ventricular arrhythmia induced haemodynamic instability
D. Contraindications to thrombolytic therapy
E. Patients < 50 years of age



12. Th
probab
A. M
B. H
C. D
D. O
E. I



13. Im
EXCEP
A. L
B. A
C. A
D. A
E. A


14. Ind
myoca
A. S
B. S
C. A
D. N
E. C



15. A p
follow
A. E
B. H
C. S
D. L
E. H


he followin
able time s
Minutes to
Hours to d
Days to we
Old (weeks
Impossible
mportant d
PT
Lobar pneu
Aortic diss
Acute pulm
Acute peri
Appendicit
dications
ardial inf
Successful
ST-segmen
Acute Post
New-onset
Continuing
pure right
wing signs
Elevation o
Hypotensi
Signs of pu
Low or nor
Hepatic co
ng ECG is
span sinc
o hours (ac
days (early)
eeks (interm
smonths)
e to tell
differenti
umonia
section
monary em
carditis
tis
s to restor
farction (A
l resuscitat
nt elevation
terior infar
t left bundl
g pain and
t ventricu
s EXCEPT
of the jugu
ion
ulmonary o
rmal pulm
ongestion
s taken fr
ce comple
cute)
)
mediate)
)
ial diagno
mbolism
re patenc
AMI) incl
tion after a
n > 2 mm i
rction
le branch b
d evidence o
ular infar
T
ular venous
oedema
monary wed
[62]
rom a pat
ete occlus
osis of AC
cy of the c
lude all th
all cardiac a
in V2V6
block
of evolving
rction is l
s pressure
dge pressur
tient with
sion of th
CS includ
coronary
he follow
arrests
g infarction
likely to p

re
h ACS; wh
he corona

es all of t
arteries i
wing EXCE
n 1224 ho
present w
Self-assess
hat is the
ary artery
the follow
in acute
EPT
ours after o
with any o
sment

y?
wing
onset
of the
Self-assessment
[63]



Self-assessment answers

Type K

Q1.

Q2.

Q3.

Q4.

Q5.

Q6.

Q7.

Q8. Q9. Q10.
A. T
B. F
C. T
D. T

A. F
B. F
C. T
D. T

A. F
B. F
C. T
D. F

A. F
B. T
C. T
D. F

A. T
B. F
C. T
D. F

A. F
B. F
C. F
D. T

A. F
B. T
C. F
D. T

A. T
B. T
C. F
D. F

A. T
B. F
C. T
D. T

A. F
B. T
C. T
D. F




Type A
11. Answer E is correct
12. Answer A is correct
13. Answer E is correct
14. Answer A is correct
15. Answer C is correct


PAT

A 50-y
histor
experie
night. T
He has
blocker
ten ciga

Q. Give
home f

A. No. H
rest and
(ACS).


Q. How

A. He s
monito
ECG do
setting
classica


Feature

Concep

Risk fa

Q. How
stable e

A. Acut
rupture

Pathop


D

TIENT
year-old m
ry of inter
enced while
The discom
a five-year
r therapy. H
arettes a da
en his norm
for outpatie
His pain h
d with min

w should he
should be a
ored, shoul
oes not hav
. Even had
al and its o
es of ischae
pt of acute
ctors for co
w is the pat
exertional
te coronary
e and throm
physiology
avies MJ. T
3613
CHAL
man atten
rmittent e
e mowing t
mfort is ass
r history o
He has no
ay for 30 y
mal ECG an
ent assessm
history is ty
nimal exert
e be manag
admitted to
ld have ser
ve sufficien
d he lacked
occurrence

emic chest
coronary s
oronary ath
thophysiolo
chest pain
y syndrom
mbus form

of ACS
The pathoph
366. PMID
LLENG
nds the em
episodes
the lawn, i
sociated wi
f hyperten
family hist
years. His E
nd his lack
ment?
ypical of isc
tion gives h
ged? Does
o a coronar
ial ECGs a
nt predictiv
risk factor
suggests h
t pain
syndrome (
herosclero
ogy of his p
?
mes usually
mation resu
hysiology of
10677422
[64]
GES
mergency
of centra
it now occu
ith heavine
nsion and h
tory of isch
ECG on pre
k of a famil
chaemic ch
him the dia
a normal E
ry care uni
and serial t
ve value to
rs (cigarett
him to be a
(ACS)
osis
presentatio
occur as a
ulting in pa
f acute coro
y departm
al chest di
urs at rest a
ess of his le
has been no
haemic hea
esentation
y history is
hest pain a
agnosis of
ECG exclud
it (CCU) an
roponin m
o exclude m
te abuse, h
at high risk
on differen
result of th
artial or com
nary syndro
ment with
iscomfort
and has aw
eft arm and
on-complia
art disease
is normal.
s it approp
nd its rece
acute coro
de the diag
nd should b
measuremen
myocardial
hypertensio
k.
nt to that o
he develop
mplete ves
omes. Heart
Patient Chall
h a week l
rt. First
wakened hi
d mild dysp
ant with hi
e. He has sm
.
priate to se
ent occurre
onary synd
gnosis of A
be continu
nts. A norm
infarction
on) his pain
of a patient
pment of pl
ssel occlusi
t 2000; 83:
lenges
long
im at
pnoea.
is -
moked
nd him
ence at
rome
AMI?
uously
mal
in this
n is
with
laque
ion.



You un
signific
observa

Q. Wha

A. Ther
cardiac
Serial e
angina

Biochem

Followi
episode
his infe
the dev

Risk str

Q. Wha

A. Such
thienop
ischaem
necessa
need fo
hospita

strategi

He und
artery w
procedu
continu

Use of a

Four y
central
non-co
with pu
per min
clear. O
is obtai
door-to
nderstand t
cant risk an
ation and t
at treatmen
rapy is dire
c ischaemia
estimation
are used t
mical mark
ing admiss
es of chest
erior leads.
velopment
ratification
at therapie
h high risk
pyridine, fu
mia treatm
ary other a
or emergen
al discharg
An under
ies and acu
dergoes cor
with placem
ure and he
uing therap
angioplast
years late
l chest disc
ompliant w
ulse 90 per
nute. The h
Oxygen is a
ined (see b
o-balloon t
that the on
nd decide t
treatment.
nt and inve
ected at pa
a (re-instit
of cardiac
o quantita

kers
sion, tropo
discomfor
. The recur
of ECG ch

n of ACS
es should b
factors req
ull heparin
ments (intra
anti-angina
nt angiogra
ge.
rstanding o
ute manag
ronary ang
ment of a b
e is able to
py, 48 hou

ty and sten
er, now ag
comfort in
with medica
r minute, b
heart soun
applied by
below) and
time is 23
nset of new
to admit hi

estigations
acifying pla
tution of hi
c biomarker
te risk and
onin rises to
rt and on o
rrence of ch
anges sugg
e administ
quire furth
nization +/
avenous nit
al agents).
aphy and d
of pathoph
ement of n
giography a
bare metal
be dischar
rs after thi
nts
ged 54, he
association
ation. Exam
blood press
ds are norm
face mask
blood is d
3 hours.
[65]
w ischaemic
im to the c
s should be
aque (aspi
is -blocke
rs, serial E
d to guide t
o twice nor
one occasio
hest pain,
gest that th
tered at thi
her treatme
/ a GP IIb
trates plus
Failure of
definitive tr
hysiology e
non-STEM
and PCI of
stent. His
rged to the
is.
e presents w
n with dysp
mination re
sure 150/9
mal with n
and an int
drawn for tr
c chest pain
coronary ca
e commenc
irin and he
er). Subling
ECGs and o
therapy.
rmal. He e
on develops
elevation o
he patient i
is stage?
ent to cont
b/IIIa block
s titration o
these featu
reatment o
nhances kn
I and unst
f an 80% st
symptoms
e ward 24 h
with a one
pnoea and
eveals an a
5 mmHg, a
no murmur
travenous c
roponin m
n identifies
are unit (CC
ced?
eparin) and
gual nitrate
observation
experiences
s ST-segme
of cardiac b
is at high r
rol plaque
ker) and fu
of -blocke
ures to reso
of any steno
nowledge o
able angin
tenosis of h
s settle wel
hours later
-hour histo
nausea. H
anxious, dia
and respira
rs and the l
cannula is
measuremen
Patient Chall
s a patient
CU) for clo
d at moder
es are char
n for recurr
s four furth
ent depres
biomarker
risk.
e (a
urther anti
ers and if
olve sugge
osis prior t
of therapeu
na (UA).
his right co
ll with this
and home
ory of seve
He has agai
aphoretic m
atory rate
lung bases
inserted. A
nt. The est
lenges
at
ose
rating
rted.
rent
her
ssion in
s and
-
sts the
to
utic
oronary
s
e, on
ere
n been
man
of 16
s are
An ECG
imated


ECG in

Corona



Q. Wha
your tre

A. The
elevatio
clinical
immed

Q. Wha

A. The
develop
placed


Risk str


D


Q. Wou
exposin

A. No. T
to a tre
(time i
is that c
nterpretatio
ary anatom
at does this
eatment op
ECG revea
on in leads
l setting of
diate coron
at is your u
likely back
ped at the s
stent is an
ratification
avies MJ. T
3613
uld it not b
ng the pati
The clinica
eatment arm
is muscle)
clinical tria

on
my
s ECG show
ptions?
als the clas
s II, III and
f ischaemic
ary reperfu
understand
kground pa
site of plaq
nother poss

n of ACS
The pathoph
366. PMID
be prudent
ent to pote
al presenta
m requirin
and are st
als have ne
w? How do
sic change
d aVF (chec
c pain and i
usion is ind
ding of the
athophysio
que ruptur
sibility.
hysiology of
10677422
to await co
entially dan
ation and E
ng acute rep
trongly ass
ever used t
[66]
oes this dia
es of inferio
ck for later
in the abse
dicated.
likely back
ology is of t
re or fissuri
f acute coro
onfirmatio
ngerous tre
ECG findin
perfusion t
sociated wi
troponins a

agnosis and
or myocard
ral and pos
ence of an
kground pa
totally occl
ing. Throm
nary syndro
on of tropon
eatments?
ngs are suff
therapy. Ti
ith worsene
as a criterio
d stratifica
dial infarct
sterior exte
alternative
athophysio
luding thro
mbosis with
omes. Heart
nin elevati

ficient to al
ime delays
ed prognos
on for repe
Patient Chall
ation deter
tion with S
ension). In
e diagnosis
ology?
ombus whi
hin the pre
t 2000; 83:
ion before
llow stratif
s are critica
sis. Anothe
erfusion.
lenges
mine
ST
n the
s,
ich has
eviously



fication
al
er point


deleter

Q. Wha

A. The
reopen
are acc
reperfu
90120
within
should
of treat

Indicat

An

Retepla
deep Q
motion
occlude
requiri

Echoca

Q. Wha

A. Ther
antipla
agent. T
infarcti
angiote
he shou
nitrogly

STEMI re
rious.
at therapy
presence o
ning of th
ceptable op
usion. STEM
0 minutes
30 minute
be transfe
tment sign
tions and c
ndersen HR
al. DA
fibrin
349(8
ase is admi
Q waves in h
n defect in t
ed right co
ng specific
ardiograph
at medicati
rapies dire
atelet agent
Therapies
ion include
ensin recep
uld be mon
ycerin shou
equires urg
is indicate
of STEMI i
he occlud
ptions, with
MI patient
should be
es. In the p
erred to a c
nificantly an

contraindic
R, Nielsen T
ANAMI-2 In
nolytic thera
8): 733742
inistered. A
his inferior
the inferoa
ronary art
c interventi

hy in acute
ions at disc
ected at pla
ts (aspirin
proven to
e angiotens
ptor blocke
nitored reg
uld be prov

gent identi
d at this st
s an indica
ded coron
h the choic
ts in whom
considered
resence of
centre capa
nd deleteri
cations for
TT, Rasmuss
nvestigators
apy in acute
2. PMID 129
Although h
r leads and
apical regio
ery and sca
ion.
myocardia
charge may
aque stabili
and clopid
improve su
sin-conver
ers (e.g. val
gularly to a
vided for s

[67]
ification an
tage?
ation for th
nary arter
ce dependin
m the time t
d for fibrin
f contraind
able of perf
iously affec
thromboly
sen K, Thue
s. A compar
e myocardia
930925
he makes u
d echocardi
on. Subseq
attered irr
al infarctio
ay improve
isation and
dogrel) and
urvival by
rting enzym
lsartan). H
achieve targ
symptomat
nd specific
herapy dire
ry. Both PC
ng largely o
to PCI is ex
nolytic ther
dications to
forming PC
ct outcome
ytic therap
esen L, Kelb
rison of coro
al infarction
uncomplica
iography d
quent angio
egularities
n
his progno
d proven to
d the introd
affecting c
me (ACE) i
His -block
get blood p
tic relief.
treatment
ected at im
CI and thro
on the exp
xpected to
rapy, which
o thrombol
CI. Delays i
e.
py
baek H, Tha
onary angio
. N Engl J M
ated progre
demonstrat
ography re
s throughou
osis?
o improve s
duction of
cardiac rem
nhibitors o
er can be r
pressure go
Patient Chall
t. Delay is
mmediate
ombolytic t
pected time
be greater
h should be
lysis, the p
in adminis
ayssen P, et
oplasty with
Med 2003;
ess, he dev
tes a region
eveals a tot
ut his LAD
survival in
a lipid-low
modelling
or possibly
recommen
oals. Sublin
lenges

therapy
e to
r than
e given
atient
stration


h
velops
nal wall
ally
D not
nclude
wering
post-
y
ced and
ngual

Q. Wha

A. He s
hospita
not sett
recurre

Adjunc


Severa
hour hi
shown.


Q. Inte

A. Ther
indicat
consist
patient
myocar
he is cle

ECG in

Examin
minute
examin
beat or
and coo

Physica

Link to
at general l
should ceas
al should h
tle rapidly
ence of sten
ctive therap
al years la
istory of op
.
rpret the E
re is extens
ting new ST
tent with h
ts previous
rdium thre
early at ris
nterpretatio
nation reve
e, blood pre
nation show
r point of m
ol extremit
al examina
o PACT mo
lifestyle ad
se smoking
he experien
with GTN
nosis.

pies in STE
ater, the p
ppressive c
ECG findin
sive and sig
TEMI. The
is known p
s inferior m
eatened by
sk.

on and cor
eals him to
essure 90/
ws wheezin
maximal im
ties.

ation of my
odule on He
dvice shoul
g and main
nce similar
. Periodic r
EMI
patient pre
chest disco
ngs
gnificant e
ere are Q w
previous in
myocardial
new and e
onary arte
o be ashen
/60 mmHg
ng and bila
mpulse (PM
yocardial in
eart failure
[68]
ld he be giv
ntain ideal
discomfor
review may
esents to th
omfort and
elevation of
waves in the
nferior infa
l infarction
evolving my
ery anatom
(grey) and
g and respi
ateral rales
MI), an S3 g
nfarction
e
ven?
body weig
rt with min
y be of use
he emergen
d shortness
f ST-segme
e inferior le
arction. Fro
n and from
yocardial i
my
d in acute d
ratory rate
s, a diffuse
gallop, a ho
ght. He sho
nimal exert
e in predict
ncy departm
of breath.
ents in lead
eads (II, II
om our kno
the extent
infarction,
distress, wi
e of 36 per
and latera
olosystolic
Patient Chall
ould presen
tion or tha
ting the
ment with
. His ECG i

ds V1V4
II, aVF)
owledge of
t of anterio
we recogn
ith pulse 13
minute. Ph
ally displac
c apical mu
lenges
nt to
t does
a two-
is
f this
or
nise that
30 per
hysical
ed apex
urmur


Q. Wha

A. It is

Q. Why
history

A. Card
multive
normal
myocar
previou
of acute


Risk fa

Pathop

Q. Wha

A. Relie
excessi
Central
resusci

Oxygen
ventilat
stabilis
non-inv

Arrhyth
prompt
blood p
evaluat
ischaem

Manag

Invasiv

Increas
mechan
(ABG)
12, Sa
hypoten
mean a
oedema
at is this m
critical to
y has this c
y relevant?
diogenic sh
essel coron
lly develop
rdial infarc
us inferior
e anterior
ctors for ca
physiology
at immedia
ef of pain a
ive sympat
l venous an
itation shou
nation and
tion may b
sation befo
vasive vent
hmias may
tly with an
pressure an
tion. These
mia causin
ement of c
ve cardiac m
sing hypox
nical ventil
are pH 7.1
aO2 95% on
nsion wors
arterial blo
a.
man's diagn
recognise t
complicatio

hock is mos
nary diseas
ps in myoca
ction, and t
infarction
infarction.

ardiogenic
of cardioge
ate manage
and anxiety
hetic activ
nd arterial
uld be con
airway pro
be required
ore cardiac
tilation (N
y have majo
nti-arrhythm
nd tissue p
e are tempo
g hypotens

cardiogenic
monitoring
xia refracto
lation to d
2, pCO2 44
n FiO2 of 0
sens and h
od pressur
nosis? Is ea
that this m
on of myoc
st often ass
se. This is i
ardial segm
this respon
has likely
.
c shock
enic shock
ement step
y with mor
vity and dec
access, an
sidered un
otection ar
d to reduce
catheterisa
NIPPV) first
or effects o
mic drugs,
perfusion sh
orising, bu
sion, which
c shock
g
ory to NIPP
ecrease wo
4 mmHg (5
0.6 and 8 c
he requires
re of 60 mm
[69]
arly diagno
man has car
cardial infa
sociated w
important
ments that
nse helps m
limited his
k
ps should b
rphine (or
creases oxy
nd pulse ox
nless frank
re critical.
e work of br
ation. In th
t.
on cardiac
, cardiover
hould be in
ut vital to re
h in turn w
PV requires
ork of brea
5.8 kPa), p
cm PEEP. D
norepinep
mHg. His c
osis import
rdiogenic s
arction occ
with anterio
because co
are not inv
maintain ca
s ability to
be undertak
fentanyl if
ygen dema
ximetry are
pulmonar
Intubation
reathing an
his instanc
output and
rsion or pac
nitiated co
everse the
worsens isc
s intubatio
athing. Res
pO2 70 mm
Despite a f
phrine 0.1 m
chest X-ray
ant?
shock.
curred? Is h
or myocard
ompensato
volved in a
ardiac outp
compensa
ken?
f hypotensi
and, preloa
e indicated
ry oedema
n and mech
nd facilitat
ce you elect
d should be
cing. Meas
ncomitant
vicious cyc
haemia.
on and intr
ults of arte
mHg (9.3 kP
fluid challe
mcg/kg/m
y (CXR) sh
Patient Chall
his previou
dial infarcti
ory hyperki
an acute
put. In this
ate in the s
ive) reduce
ad and afte
d. Cautious
is present.
hanical
te sedation
t for a trial
e corrected
sures to ma
tly with dia
cle of myoc
roduction o
erial blood
kPa), Base E
enge his
min to main
hows pulm
lenges
us
ion and
inesis
s case,
etting
es
erload.
fluid
.
n and
l of
d
aintain
agnostic
cardial
of
gas
Excess
ntain a
monary


Differe

Q. Wha
remem

A. Echo
cardiog
echocar
(pulmo
echocar
ventric


Q. If a p
haemod

A. Yes,
clinical
myocar
can cha

Echoca
Invasiv
PACT m

Q. Wha

A. Nitra
persisti
remain
contrac
heart ra
milrino
Continu

Q. Intra
physiol

A. IABP
increas
effects,
increas

Vasoac
Heart f
Link to

ential diagn
at further d
mbering tha
ocardiogra
genic shock
rdiography
onary flotat
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cular infarc
pulmonary
dynamic m
it often is
l estimates
rdial perfo
ange cardia
ardiograph
ve haemody
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at further p
ates and af
ing hypote
ns inadequa
ctility and
ate and res
one may be
uation of n
a-aortic ba
logical ben
P reduces s
sing cardia
, in contras
se in oxyge
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failure man
o PACT mo

nosis of the
diagnostic
at treatmen
aphy is an e
k and rulin
y should be
tion cathet
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ction and m
y artery flo
managemen
more usefu
s of filling p
rmance an
ac output a

hy
ynamic mo
Haemody
pharmacol
fterload re
ension and
ate. An ino
cardiac ou
sponse to a
e considere
noradrenal
alloon pum
nefit might
systolic aft
ac output an
st to those
n demand

py in cardio
nagement
odule on He
e patient w
procedure
nt is ongoin
excellent in
ng out othe
e routine. I
ter) may be
adily availa
mechanical
otation cath
nt?
ful to optim
pressure ca
nd complia
and filling
onitoring
ynamic mon
ogic measu
duction ar
diuretics a
otropic age
utput. Choic
a trial of th
ed, if the pa
line may be
mp counterp
it bring to
terload and
nd improv
of inotrop
.
ogenic sho
eart failure
[70]
with shock
es should b
ng?
nitial tool f
er causes of
Invasive ha
e useful dia
able, to exc
l complicat
heter is pla
mise therap
an be unrel
ance and th
pressures
nitoring
ures are in
re difficult
are unlikel
ent such as
ce of agent
herapy and
atient is no
e required
pulsation (
o this situat
d augment
ving corona
ic or vasop
ock
e
be consider
for confirm
f shock; th
aemodyna
agnosticall
clude volum
tions of my
aced, has it
py in unsta
liable, and
he related t
rapidly.
ndicated or
to introdu
ly to be effe
dobutami
t is depend
d agents suc
ot excessiv
if hypoten
(IABP) ma
tion?
s diastolic
ary blood fl
pressor age
red at this s
ming the dia
erefore ear
mic monit
ly, especial
me depletio
yocardial in
t a useful ro
ble patient
d because c
therapeutic
may be co
ce here bec
ective given
ne may inc
dent upon b
ch as levos
vely hypote
nsion persis
ay be indica
perfusion
low. These
ents, occur
Patient Chall
stage
agnosis of
rly
toring
lly if exper
on, right
nfarction.
ole in ongo
ts, because
changes in
c intervent
onsidered?
cause of
n that perf
crease
blood pres
simendan a
ensive.
sts.
ated. What
pressure t
e beneficial
r without a
lenges

rt

oing
e

tions

fusion
ssure,
and
t
hus
l
n

Echoca
infarcti
functio
rupture
PAOP 3

Mitral r

Q. Wha

A. Whil
used al
stenosi
therape
treatme

Q. Wha

A. Card
patient
grafting
been sh
If haem
therapy
recover

Percuta

Outcom

On ref
ischaem
during
biomar
optima
immed
offered
stratific
medica
angiopl

Random
the imm
myocar
be fami
patient
Cardiog
and req
acute re

ardiograph
ion, antero
on. There is
e. Pulmona
32, CI 1.9.
regurgitati
at clinical b
le IABP is
lone it does
is. IABP is
eutic meas
ent.
at should b
diac cathet
t. Emergen
g (CABG) i
hown to co
modynamic
y, left ventr
ry.
aneous cor
me from ca
flection, t
mic heart d
its evoluti
rkers and c
al therapy.
diate revasc
d. Patients w
cation tech
al therapy a
lasty or ste
mised cont
mediate, in
rdial infarc
iliar with a
ts can be ob
genic shoc
quires rapi
evascularis
hy shows an
o-apical ak
s mild mitr
ary artery c
Dobutami

ion
benefit has
efficacious
s not subst
best regar
sures to be
be done now
erisation w
ncy revascu
if warrante
onsistently
c instability
ricular ass

ronary inte
ardiogenic
the clinic
disease and
on. The dia
clinical inte
Patients pr
cularisation
without ST
hniques are
and those w
ent insertio
trolled tria
ntermediat
ction. Clini
all these int
btained by
ck is perhap
id recognit
sation.
n akinetic a
inesis, and
ral regurgit
catheter re
ne is added
s IABP in th
s for initial
tantially im
ded as an e
undertake
w to impro
with revasc
ularisation,
ed by coron
reduce mo
y persists d
ist device t
erventions
shock
cal course
d the differ
agnosis of
egration be
resenting w
n therapy w
T elevation
e required
who requir
on.
als have det
te and long
icians invo
tervention
y recognitio
ps the mos
ion, stabili
[71]
and fibroti
d severely d
tation but
esults revea
d to norep
his situatio
l stabilisati
mprove blo
essential su
en rather th
ove the like
cularisation
, with eithe
nary anato
ortality rat
despite rep
therapy ma

e of this p
rent interve
ACS is a m
eing requir
with STEM
with attend
n may still b
to ascertai
re immedia
termined a
g-term prog
olved in acu
ns. Improve
on of the co
st feared co
isation wit
ic inferior w
depressed l
no evidenc
al RAP 10,
inephrine
on and wha
ion of patie
ood flow dis
upport me
han an ind
elihood of
n if approp
er PCI or c
omy, is the
es in patie
perfusion, I
ay be cons
patient illu
entions req
medical em
red to asse
MI require e
dant impro
be at consi
in those wh
ate angiogr
a number o
gnosis of p
ute and cri
ement in th
omplicatio
omplication
th medical
wall indica
left ventric
ce of papill
RVP 50/12
and an IAB
at are its li
ents with c
stal to a cri
chanism to
dependent m
survival?
priate is ess
oronary ar
only interv
nts with ca
IABP, and
idered as a
ustrates a
quired at v
mergency wi
ss risk and
early recog
ovement in
iderable ris
ho will sett
raphy and
of therapie
people suffe
tical care m
he survival
ns of myoc
n of myoca
therapy an
Patient Chall
ative of old
cular systo
lary muscl
2, PAP 50/
BP is place
imitations?
cardiogenic
itical coron
o allow def
modality o
sential in t
rtery bypas
vention tha
ardiogenic
pharmaco
a bridge to
a spectrum
varying stag
with ECGs, s
d to provid
gnition so t
n survival,
sk and
tle best wit
possible
es that imp
fering acute
medicine n
l of specific
cardial infa
ardial infar
nd ultimate
lenges
d
olic
e
/34,
ed.
?
c shock,
nary
finitive
of
this
ss
at has
shock.
ologic

m of
ges
serial
e
that
can be
th
prove
e
need to
c
arction.
rction
ely