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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 Schröder
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
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itchett D, Gcoron1309–http:/
d out more
Anbe DT, AAHA guidelardial infarology/Ame
elines (Comtients with A292. PMID
americanhe
L, Adams CDAHA 2007
na/non ST-ege of Cardioelines. Circuable http://circ.1
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mmittee to RAcute Myoc 15339869
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D, Antman E guidelines felevation myology/Amerulation 200
.ahajournal
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aj.ca/cgi/rep
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Hand M, A007 focused agement of Pt of the AmForce on Prdian Cardioly Physiciante the ACC/ST-Elevationg Committ
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2007 Focuseutaneous Co Focused Updation/Ameelines. Circu
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SFER-AMI s for STEMdiately afteful or not. , heart fail.2% in pati
Borgundvaagioplasty afgl J Med 20
pitals that repatterns of tere admitted
[27]
nt choice amitting hos
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PW, Bates Ethe ACC/AHth ST-Elevaege of Cardidelines: devociety endorriting Group Guidelinesial Infarctio
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, King SB IIC/AHA Guid
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sen K, Thuery angioplasngl J Med 20
G, Sanborn Tcute myocarInvestigatornaries for cID 1046081
rimary angiute myocardals. Lancet
rcia E, Tcheng, with or wingl J Med 20
berg O, EcoIa inhibitionngl J Med 20
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ntman EM,EnoxaelevatPMID
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, Cannon CPal; CLARITYin and fibrintion. N Engl
R, Berger PBtigators. Ea
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Brouwer MAse. Heart 20
nated (UFLMWH) a
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ated heparieteplase or anti-thrombnless the r
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Morrow DAaparin versution myocar
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P, Gibson CY-TIMI 28 Inolytic therl J Med 200
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A, McCabe us unfractiordial infarct
enez-Silva Ja-analysis o92; 327(4):
[34]
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rapy for myo05; 352(12)
III, Fry ET,stained dualrvention: a PMID 1243
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harmacokin of the aPTy and are leeous admin
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CH, Murphonated hepation. N Engl
J, Kupelnicof therapeut
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Sendón JL, rs. Additionocardial infa: 1179–1189
, DeLago A,l oral antipl randomized35254
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er B, Guagling primary 21): 2218–2
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jta J, Hubermes. Heart
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ht P. Aspirinial infarctio
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HORIZONSment with routine us30 days, ow
%).
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ating to an
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reatment; hvation myoction (STEMtion for usenitoring the
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nhibitor; lonanagement,contraindic
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R, Collins R, 852 patientslled trial. La
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[38]
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ise Textbook pp. 256–26
CT modulee AMI and
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, Crea F, Magina. N Engl
n-ischaemind acute pu
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ecreased mynfarct arterypressure or other than
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anagement mary – ACCpes DP, Libb
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isation
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[39]
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v.)
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ed medicalntra-aortic improving cted to be b
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(CABG) shse, three-v
of Chronic C/AHA Cardby P, editorth ed. Phila
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ecompensaidered. Echis group of
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hannel bloc
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risation. PCg that acutelective an
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ation after hocardiogr conditions
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ent of complica
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se: AHA/ACmaries. In:
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[40]
Use of right heart catheterisation and echocardiography in diagnosis
DIAGNOSIS CVP PAOP CO OTHER
FINDINGS ON PAC
ECHOCARDIOGRAPHY
Mechanical complications
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 infarction or
normal
RV dysfunction
Pump failure (cardiogenic
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 Presentation 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 3–5 days. Free wall rupture presents as a catastrophic event with shock and electromechanical dissociation.
Thwthaf
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Cardiol 200
ular sept
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nce of ventrin the throseptal rupt shock, wit
hallmark finn SvO2 fromartery cathventricular
th can prodesult from most easilt heart cath
ment
epair is theure may occreated veryapidly enlah IABP, vade), when turgery has epair shoulof a percutatients.
an elderly f Early repeac rupture,ctually incr
th free walnd surgicalcan help mchocardiogr
onelli TA, Mdiac free-waction: a repscularize oc0: 36(3 Sup
tal ruptu
ricular septombolysis eture presenth a pansysnding is a l
m right atriheter tracinr septal rup
duce drama increased ly made wiheterisatio
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[41]
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make the diaraphy’ abo
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port from thccluded coroppl A): 1117–
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chocardiogncludes freump failuratheterisat
Managem
emporising Afte Intr Ino
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atson JD. In2008. ISBN
ebb JG, Hilprofile of venardial infar
mergently reColl Cardiol
Fishbein M myocardial
D 12409546
ptimal man2): 1462–146
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MC, Blanchel infarction.
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[42]
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tricular sept
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[53]
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Montalescoinolytic ther N Engl J M
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DJ, Smith Hng thrombollts of the Thlation 1991;
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ot G, Therourapy for
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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 15–30% 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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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 250–500 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 8–10 % B. Ventricular arrhythmias C. Sudden hypertensive episodes (Bezold–Jarisch 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/m2 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. Thprobab
A. MB. HC. DD. OE. I
13. ImEXCEP
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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-yhistorexperienight. THe has blockerten ciga Q. Givehome f A. No. Hrest and(ACS). Q. How A. He smonitoECG dosettingclassica
Feature Concep Risk fa Q. Howstable e A. Acutrupture
Pathop
D
TIENT
year-old mry of interenced whileThe discom a five-yearr therapy. Harettes a da
en his normfor outpatie
His pain hd with min
w should he
should be aored, shouloes not hav. Even hadal and its o
es of ischae
pt of acute
ctors for co
w is the patexertional
te coronarye and throm
physiology
avies MJ. T361–3
CHAL
man attenrmittent ee mowing t
mfort is assr history oHe has no ay for 30 y
mal ECG anent assessm
history is tynimal exert
e be manag
admitted told have serve sufficien
d he lackedoccurrence
emic chest
coronary s
oronary ath
thophysiolo chest pain
y syndrommbus form
of ACS
The pathoph366. PMID
LLENG
nds the emepisodes the lawn, i
sociated wif hyperten family histyears. His E
nd his lackment?
ypical of isction gives h
ged? Does
o a coronarial ECGs a
nt predictiv risk factor suggests h
t pain
syndrome (
herosclero
ogy of his p?
mes usually mation resu
hysiology of10677422
[64]
GES
mergency of centrait now occuith heavine
nsion and htory of ischECG on pre
k of a famil
chaemic chhim the dia
a normal E
ry care uniand serial tve value tors (cigaretthim to be a
(ACS)
osis
presentatio
occur as aulting in pa
f acute coro
y departmal chest diurs at rest aess of his lehas been nohaemic heaesentation
y history is
hest pain aagnosis of
ECG exclud
it (CCU) anroponin m
o exclude mte abuse, hat high risk
on differen
result of thartial or com
nary syndro
ment withiscomfortand has aweft arm andon-compliaart disease is normal.
s it approp
nd its rece acute coro
de the diag
nd should bmeasuremenmyocardial hypertensiok.
nt to that o
he developmplete ves
omes. Heart
Patient Chall
h a week lrt. First wakened hid mild dyspant with hi
e. He has sm.
priate to se
ent occurreonary synd
gnosis of A
be continunts. A norm infarctionon) his pain
of a patient
pment of plssel occlusi
t 2000; 83:
lenges
long
im at pnoea. is β-moked
nd him
ence at rome
AMI?
uously mal in this n is
with
laque ion.
You unsignificobserva Q. Wha A. ThercardiacSerial eangina
Biochem Followiepisodehis infethe dev
Risk str Q. Wha A. Suchthienopischaemnecessaneed fohospita
strategi He undartery wproceducontinu
Use of a Four ycentralnon-cowith puper minclear. Ois obtaidoor-to
nderstand tcant risk anation and t
at treatmen
rapy is direc ischaemiaestimation are used t
mical mark
ing admisses of chest erior leads.velopment
ratification
at therapie
h high risk pyridine, fumia treatmary other aor emergenal discharg
An underies and acu
dergoes corwith placemure and heuing therap
angioplast
years latel chest discompliant wulse 90 pernute. The hOxygen is ained (see bo-balloon t
that the onnd decide ttreatment.
nt and inve
ected at ‘paa (re-instit of cardiaco quantita
kers
sion, tropo discomfor. The recur of ECG ch
n of ACS
es should b
factors requll heparin
ments (intraanti-anginant angiograge.
rstanding oute manag
ronary angment of a be is able to py, 48 hou
ty and sten
er, now agcomfort in
with medicar minute, bheart sounapplied by below) and time is 2–3
nset of newto admit hi
estigations
acifying platution of hic biomarkerte risk and
onin rises tort and on orrence of changes sugg
e administ
quire furthnization +/avenous nital agents). aphy and d
of pathophement of n
giography abare metal be discharrs after thi
nts
ged 54, heassociation
ation. Examblood pressds are normface mask blood is d
3 hours.
[65]
w ischaemicim to the c
s should be
aque’ (aspiis β-blockers, serial E
d to guide t
o twice norone occasiohest pain, gest that th
tered at thi
her treatme/– a GP IIbtrates plus Failure of
definitive tr
hysiology enon-STEM
and PCI of stent. Hisrged to theis.
e presents wn with dyspmination resure 150/9mal with n and an int
drawn for tr
c chest paincoronary ca
e commenc
irin and heer). SublingECGs and otherapy.
rmal. He eon developselevation o
he patient i
is stage?
ent to contb/IIIa blocks titration o these featureatment o
nhances knI and unst
f an 80% st symptoms
e ward 24 h
with a onepnoea andeveals an a5 mmHg, a
no murmurtravenous croponin m
n identifiesare unit (CC
ced?
eparin) andgual nitrateobservation
experiencess ST-segmeof cardiac bis at high r
rol plaque ker) and fuof β-blockeures to resoof any steno
nowledge oable angin
tenosis of hs settle wel
hours later
-hour histo nausea. H
anxious, diaand respirars and the lcannula is
measuremen
Patient Chall
s a patient CU) for clo
d at moderes are charn for recurr
s four furthent depresbiomarkerrisk.
e (a urther antiers and if olve suggeosis prior t
of therapeuna (UA).
his right coll with this and home
ory of seveHe has agai
aphoretic matory rate lung bases inserted. Ant. 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. Whayour tre A. The elevatioclinicalimmed Q. Wha A. The developplaced
Risk str
D
Q. Wouexposin A. No. Tto a tre(‘time iis that c
nterpretatio
ary anatom
at does thiseatment op
ECG reveaon in leadsl setting of
diate coron
at is your u
likely backped at the s stent is an
ratification
avies MJ. T361–3
uld it not bng the pati
The clinicaeatment armis muscle’) clinical tria
on
my
s ECG showptions?
als the class II, III andf ischaemicary reperfu
understand
kground pasite of plaq
nother poss
n of ACS
The pathoph366. PMID
be prudent ent to pote
al presentam requirin and are stals have ne
w? How do
sic changed aVF (checc pain and iusion is ind
ding of the
athophysioque ruptursibility.
hysiology of10677422
to await coentially dan
ation and Eng acute reptrongly assever used t
[66]
oes this dia
es of inferiock for laterin the absedicated.
likely back
ology is of tre or fissuri
f acute coro
onfirmationgerous tre
ECG findinperfusion t
sociated witroponins a
agnosis and
or myocardral and posence of an
kground pa
totally occling. Throm
nary syndro
on of troponeatments?
ngs are sufftherapy. Tiith worseneas a criterio
d stratifica
dial infarctsterior extealternative
athophysio
luding thrombosis with
omes. Heart
nin elevati
ficient to alime delaysed prognoson for repe
Patient Chall
ation deter
tion with Sension). Ine diagnosis
ology?
ombus whihin the pre
t 2000; 83:
ion before
llow stratifs are criticasis. Anotheerfusion.
lenges
mine
ST n the s,
ich has eviously
fication al er point
deleter Q. Wha A. The reopenare accreperfu90–120within should of treat
Indicat
An
Retepladeep Qmotionoccluderequiri
Echoca Q. Wha A. Therantiplaagent. Tinfarctiangiotehe shounitrogly
STEMI rerious.
at therapy
presence oning of th
ceptable opusion. STEM0 minutes 30 minute be transfetment sign
tions and c
ndersen HRal. DAfibrin349(8
ase is admiQ waves in hn defect in ted right cong specific
ardiograph
at medicati
rapies direatelet agentTherapies ion includeensin recepuld be monycerin shou
equires urg
is indicate
of STEMI ihe occludptions, withMI patientshould be
es. In the perred to a cnificantly an
contraindic
R, Nielsen TANAMI-2 Innolytic thera8): 733–742
inistered. Ahis inferiorthe inferoaronary art
c interventi
hy in acute
ions at disc
ected at plats (aspirin proven to e angiotensptor blockenitored reguld be prov
gent identi
d at this st
s an indicaded coronh the choicts in whomconsideredresence of
centre capand deleteri
cations for
TT, Rasmussnvestigatorsapy in acute2. PMID 129
Although hr leads andapical regioery and scaion.
myocardia
charge may
aque stabili and clopidimprove susin-converers (e.g. valgularly to avided for s
[67]
ification an
tage?
ation for thnary arterce dependin
m the time td for fibrinf contraindable of perfiously affec
thromboly
sen K, Thues. A compare myocardia930925
he makes ud echocardion. Subseqattered irr
al infarctio
ay improve
isation anddogrel) andurvival by rting enzymlsartan). H
achieve targsymptomat
nd specific
herapy direry. Both PCng largely oto PCI is ex
nolytic therdications toforming PCct outcome
ytic therap
esen L, Kelbrison of coroal infarction
uncomplicaiography d
quent angioegularities
n
his progno
d proven tod the introdaffecting c
me (ACE) iHis β-blockget blood ptic relief.
treatment
ected at imCI and throon the expxpected to rapy, whicho thrombolCI. Delays ie.
py
baek H, Thaonary angio. N Engl J M
ated progredemonstratography res throughou
osis?
o improve sduction of
cardiac ‘remnhibitors oer can be r
pressure go
Patient Chall
t. Delay is
mmediateombolytic t
pected time be greaterh should belysis, the pin adminis
ayssen P, et oplasty withMed 2003;
ess, he devtes a region
eveals a totut his LAD
survival in a lipid-lowmodelling’ or possiblyrecommenoals. 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 shospitanot settrecurre
Adjunc Severahour hishown.
Q. Inte A. Therindicatconsistpatientmyocarhe is cle
ECG in Examinminuteexaminbeat orand coo
Physica Link to
at general l
should ceasal should htle rapidly ence of sten
ctive therap
al years laistory of op.
rpret the E
re is extensting new STtent with ht’s previousrdium threearly at ris
nterpretatio
nation revee, blood prenation showr point of mol extremit
al examina
o PACT mo
lifestyle ad
se smokinghe experien with GTNnosis.
pies in STE
ater, the pppressive c
ECG findin
sive and sigTEMI. Theis known ps inferior meatened by sk.
on and cor
eals him toessure 90/ws wheezin
maximal imties.
ation of my
odule on He
dvice shoul
g and mainnce similar . Periodic r
EMI
patient prechest disco
ngs
gnificant eere are Q wprevious inmyocardial new and e
onary arte
o be ashen /60 mmHgng and bila
mpulse (PM
yocardial in
eart failure
[68]
ld he be giv
ntain ideal discomforreview may
esents to thomfort and
elevation ofwaves in thenferior infal infarctionevolving my
ery anatom
(grey) andg and respiateral rales
MI), an S3 g
nfarction
e
ven?
body weigrt with miny be of use
he emergend shortness
f ST-segmee inferior learction. Fron and fromyocardial i
my
d in acute dratory rate
s, a diffuse gallop, a ho
ght. He shonimal exerte in predict
ncy departm of breath.
ents in leadeads (II, IIom our kno the extent
infarction,
distress, wie of 36 per and lateraolosystolic
Patient Chall
ould presention or thating the
ment with . His ECG i
ds V1–V4 II, aVF) owledge oft of anterio we recogn
ith pulse 13 minute. Ph
ally displacc 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. Whyhistory A. Cardmultivenormalmyocarpreviouof acute
Risk fa Pathop Q. Wha A. RelieexcessiCentralresusci Oxygenventilatstabilisnon-inv Arrhythpromptblood pevaluatischaem
Manag Invasiv Increasmechan(ABG) −12, Sahypotenmean aoedema
at is this m
critical to
y has this cy relevant?
diogenic shessel coronlly developrdial infarcus inferior e anterior
ctors for ca
physiology
at immedia
ef of pain aive sympatl venous anitation shou
nation and tion may b
sation befovasive vent
hmias maytly with anpressure antion. Thesemia causin
ement of c
ve cardiac m
sing hypoxnical ventilare pH 7.1
aO2 95% onnsion wors
arterial bloa.
man's diagn
recognise t
complicatio
hock is mosnary diseasps in myocaction, and t infarction infarction.
ardiogenic
of cardioge
ate manage
and anxietyhetic activnd arterialuld be con
airway probe requiredore cardiac tilation (N
y have majonti-arrhythmnd tissue pe are tempog hypotens
cardiogenic
monitoring
xia refractolation to d2, pCO2 44n FiO2 of 0sens and hod pressur
nosis? Is ea
that this m
on of myoc
st often assse. This is iardial segmthis respon has likely .
c shock
enic shock
ement step
y with morvity and dec
access, ansidered un
otection ard to reduce catheterisa
NIPPV) first
or effects omic drugs,
perfusion shorising, busion, which
c shock
g
ory to NIPPecrease wo4 mmHg (50.6 and 8 c
he requires re of 60 mm
[69]
arly diagno
man has car
cardial infa
sociated wimportant ments that nse helps m limited his
k
ps should b
rphine (or creases oxy
nd pulse oxnless frank
re critical. e work of bration. In tht.
on cardiac , cardioverhould be in
ut vital to reh in turn w
PV requiresork of brea5.8 kPa), pcm PEEP. D norepinepmHg. His c
osis import
rdiogenic s
arction occ
with anterio because co are not invmaintain cas ability to
be undertak
fentanyl ifygen dema
ximetry are pulmonar
Intubationreathing anhis instanc
output andrsion or pacnitiated coeverse the
worsens isc
s intubatioathing. RespO2 70 mmDespite a fphrine 0.1 mchest X-ray
ant?
shock.
curred? Is h
or myocardompensatovolved in aardiac outp compensa
ken?
f hypotensiand, preloae indicatedry oedema
n and mechnd facilitat
ce you elect
d should becing. Measncomitant vicious cychaemia.
on and intrults of arte
mHg (9.3 kPfluid challemcg/kg/my (CXR) sh
Patient Chall
his previou
dial infarctiory hyperkian acute put. In thisate in the s
ive) reducead and afted. Cautious is present.
hanical te sedationt for a trial
e correctedsures to matly with diacle of myoc
roduction oerial blood
kPa), Base Eenge his
min to mainhows 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. Wharemem A. Echocardiogechocar(pulmoechocarventric Q. If a phaemod A. Yes, clinicalmyocarcan cha
EchocaInvasivPACT m Q. Wha A. Nitrapersistiremaincontracheart ramilrinoContinu Q. Intraphysiol A. IABPincreaseffects,increas
VasoacHeart fLink to
ential diagn
at further dmbering tha
ocardiogragenic shockrdiography
onary flotatrdiography
cular infarc
pulmonarydynamic m
it often is l estimatesrdial perfoange cardia
ardiographve haemodymodule on
at further p
ates and afing hypote
ns inadequactility and ate and resone may beuation of n
a-aortic balogical ben
P reduces ssing cardia, in contrasse in oxyge
ctive therapfailure mano PACT mo
nosis of the
diagnostic at treatmen
aphy is an ek and ruliny should betion cathety is not reaction and m
y artery flomanagemen
more usefus of filling prmance anac output a
hy
ynamic mo Haemody
pharmacol
fterload reension and ate. An inocardiac ousponse to ae considerenoradrenal
alloon pumnefit might
systolic aftac output anst to those n demand
py in cardionagement
odule on He
e patient w
procedurent is ongoin
excellent inng out othee routine. Iter) may beadily availamechanical
otation cathnt?
ful to optimpressure cand compliaand filling
onitoring ynamic mon
ogic measu
duction ar diuretics a
otropic ageutput. Choica trial of thed, if the paline may be
mp counterp it bring to
terload andnd improv of inotrop.
ogenic sho
eart failure
[70]
with shock
es should bng?
nitial tool fer causes ofInvasive hae useful diaable, to excl complicat
heter is pla
mise therapan be unrel
ance and th pressures
nitoring
ures are in
re difficult are unlikel
ent such as ce of agent
herapy andatient is noe required
pulsation (o this situat
d augmentving coronaic or vasop
ock
e
be consider
for confirmf shock; thaemodynaagnosticallclude volumtions of my
aced, has it
py in unstaliable, and
he related t rapidly.
ndicated or
to introduly to be effe dobutamit is depend
d agents sucot excessiv if hypoten
(IABP) mation?
s diastolic ary blood flpressor age
red at this s
ming the diaerefore earmic monitly, especialme depletioyocardial in
t a useful ro
ble patientd because ctherapeutic
may be co
ce here becective givenne may inc
dent upon bch as levos
vely hypotension persis
ay be indica
perfusion low. Theseents, occur
Patient Chall
stage
agnosis of rly toring lly if experon, right nfarction.
ole in ongo
ts, becausechanges in c intervent
onsidered?
cause of n that perfcrease blood pressimendan aensive. sts.
ated. What
pressure te beneficialr without a
lenges
rt
oing
e tions
fusion
ssure, and
t
hus l n
EchocainfarctifunctiorupturePAOP 3
Mitral r Q. Wha A. Whilused alstenositherapetreatme Q. Wha A. Cardpatientgraftingbeen shIf haemtherapyrecover
Percuta Outcom On refischaemduring biomaroptimaimmedofferedstratificmedicaangiopl Randomthe immmyocarbe famipatientCardiogand reqacute re
ardiographion, antero
on. There ise. Pulmona32, CI 1.9.
regurgitati
at clinical b
le IABP is lone it doesis. IABP is eutic measent.
at should b
diac cathett. Emergeng (CABG) ihown to co
modynamicy, left ventrry.
aneous cor
me from ca
flection, tmic heart d its evolutirkers and cal therapy. diate revascd. Patients wcation tech
al therapy alasty or ste
mised contmediate, inrdial infarciliar with ats can be obgenic shocquires rapievascularis
hy shows ano-apical aks mild mitrary artery c Dobutami
ion
benefit has
efficaciouss not subst best regarsures to be
be done now
erisation wncy revascuif warrante
onsistently c instabilityricular ass
ronary inte
ardiogenic
the clinicdisease andon. The dia
clinical inte Patients prcularisationwithout ST
hniques areand those went insertio
trolled triantermediatction. Cliniall these intbtained by
ck is perhapid recognitsation.
n akinetic ainesis, andral regurgitcatheter rene is added
s IABP in th
s for initialtantially imded as an e undertake
w to impro
with revascularisation,ed by coron reduce moy persists dist device t
erventions
shock
cal coursed the differagnosis of egration beresenting wn therapy wT elevatione required who requiron.
als have dette and longicians invotervention
y recognitiops the mosion, stabili
[71]
and fibrotid severely dtation but
esults revead to norep
his situatio
l stabilisatimprove bloessential suen rather th
ove the like
cularisation, with eithenary anatoortality ratdespite reptherapy ma
e of this prent interve ACS is a meing requirwith STEMwith attend
n may still b to ascertaire immedia
termined ag-term progolved in acuns. Improveon of the cost feared coisation wit
ic inferior wdepressed l no evidencal RAP 10, inephrine
on and wha
ion of patieood flow disupport mehan an ind
elihood of
n if approper PCI or c
omy, is the es in patie
perfusion, Iay be cons
patient illuentions req
medical emred to asse
MI require edant improbe at consiin those whate angiogr
a number ognosis of pute and criement in thomplicatioomplicationth medical
wall indicaleft ventricce of papill RVP 50/12and an IAB
at are its li
ents with cstal to a crichanism to
dependent m
survival?
priate is essoronary ar only intervnts with caIABP, and idered as a
ustrates aquired at v
mergency wiss risk andearly recogovement iniderable risho will settraphy and
of therapiepeople suffetical care mhe survivalns of myocn of myoca therapy an
Patient Chall
ative of oldcular systolary muscl2, PAP 50/BP is place
imitations?
cardiogenicitical corono allow defmodality o
sential in trtery bypasvention thaardiogenic pharmacoa bridge to
a spectrumvarying stag
with ECGs, sd to providgnition so tn survival, sk and tle best wit possible
es that impfering acutemedicine nl of specificcardial infaardial infarnd 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