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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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Fi

ou can findeferences.

ntman EM,ACC/AmyocaCardiGuideof Pate82–2

ttp://www.a

nderson JLACC/AanginCollegGuideavailafrom:940v1

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

Goodman S, nary syndrom–1316. PMID//www.cma

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e about acu

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mmittee to RAcute Myoc 15339869

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ute coronar

PW, Bates Ee managem

port of the At Associatio

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esenter.jhtm

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rican Heart 7; 116(7):e1

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n Task Forc999 Guidelirction). Circ

ml?identifie

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eprint/CIRC

ces in the mment to riskvailable fro

9/1309.pdf

e measures an

mes in the f

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er=3004542

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CULATION

managementk. CMAJ 20m

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M, et al. T-elevation

ice Manageme04; 110(9):

2

y DE Jr, et awith unstablhe Americance on Practic616. Full tex

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ent

l. e n ce xt

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nflammatoo rupture, abrous cap tabilise plandependen

White thromccluding. Activated plahe GP IIb/Ictivation. Pvidenced b

avies MJ. T83(3)

ibby P, Ther2005;

ami S, Willesegme37(2)

idker PM, DRosuvC-rea18997

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ty of patienult from thepon disrup

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Hand M, A007 focused agement of Pt of the AmForce on Prdian Cardioly Physiciante the ACC/ST-Elevationg Committ

Hand M, S focused upST-Elevatio

2007 Focuseutaneous Co Focused Updation/Ameelines. Circu

he TRANSrombolysislity immed is successf

f death, MIpared to 17.

Fitchett D, Bine early anction. N Eng

ew the hosptreatment pke if you wets?

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ss (particury c status.

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ed Update) oronary Intepdate): a reerican Hearulation 200

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

toms er to a cardI

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PW, Bates Ethe ACC/AHth ST-Elevaege of Cardidelines: devociety endorriting Group Guidelinesial Infarctio

ation 2008;

, King SB IIC/AHA Guid

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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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Brouwer MAse. Heart 20

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CH, Murphonated hepation. N Engl

J, Kupelnicof therapeut

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, DeLago A,l oral antipl randomized35254

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reatment; hvation myoction (STEMtion for usenitoring the

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[39]

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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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patients witcentesis, anterisation ction and ec

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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

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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

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duce drama increased ly made wiheterisatio

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[41]

female witherfusion vi, but thromrease that

ll rupture il repair. Em

make the diaraphy’ abo

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port from thccluded coroppl A): 1117–

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chocardiogncludes freump failuratheterisat

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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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atson JD. In2008. ISBNardial funct

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orrected prng.

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[46]

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nitial stabilhould be asntra-aortic but signifiVasodilatorodynamic m

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atson JD. In2008. ISBNactive agents

with inadeular suppor

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0 mmHg, b

e, a phosphchanisms nic and arrhver, have thents with ten which otholus in thisequired.

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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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[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

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Self-assessment answers Type K

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Q5.

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A. T

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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