C2 Chap08 - LONGROIS

ANESTHSIE DU CARDIAQUE
POUR CHIRURGIE NON CARDIAQUE
40
Dan LONGROIS et Jean-Pol DEPOIX
Identifier les patients ayant une cardiopathie comme tant

part dans la pratique de lanesthsie et de la mdecine pri-opratoire pourrait tre justifi par: 1) le fait que la prsence dune
cardiopathie est un facteur de risque indpendant de complications pri-opratoires; 2) les changements de prise en charge
diminuent lincidence ou la gravit des complications.
Il existe des preuves que ces deux affirmations sont vraies.
Nous avons fait le choix de prsenter de manire individualise
la physiopathologie et lvaluation propratoire pour les cardiopathies les plus frquentes. La conduite de lanesthsie et la prise
en charge postopratoire ont t prsentes en commun.
pidmiologie
Donnes pidmiologiques concernant
les pathologies cardiovasculaires
Les pathologies cardiovasculaires reprsentent la premire cause
de mortalit dans les pays dvelopps, en grande partie en relation avec le vieillissement de la population [1]. Les principales
cardiopathies sont: 1) les coronaropathies; 2) les valvulopathies;
3)linsuffisance cardiaque; 4) les cardiopathies rythmiques dont
la plus frquente est la fibrillation atriale soit 1% de la population
dans les pays occidentaux [2].
Selon les statistiques nord-amricaines de 2012 [1], la prvalence des maladies cardiovasculaires chez les sujets caucasiens
de plus de 18ans est de 11,7%; 6,4% ont une coronaropathie,
23,6% une hypertension artrielle et 2,5% ont fait un accident
ischmique crbral. La prvalence est lgrement plus faible
pour les asiatiques et les hispaniques et plus importante pour les
sujets dorigine africaine et amrindienne. Les projections sont
quen 2030, environ 40 % des habitants des tats-Unis auront
une pathologie cardiovasculaire [1]. La prvalence des maladies
cardiovasculaires en Europe et en France est moindre.

la chirurgie, les complications
cardiovasculaires pri-opratoires
et le risque chirurgical
Plus de 250 millions de patients bnficient annuellement dune
chirurgie majeure (incision/excision ncessitant une anesthsie
gnrale ou locorgionale) dans le monde [3]; dans les pays dvelopps (73% des interventions chirurgicales majeures faites dans
le monde) ceci correspond 11 000 interventions par an pour
100000 habitants [3].
La dfinition des complications cardiovasculaires pri-opratoires nest pas standardise. Elle peut aller de la survenue dune
hypotension artrielle peranesthsique (jusqu 80% des patients
en fonction des seuils utiliss pour dfinir lhypotension [4] mais
dont les consquences sur les complications graves postopratoires restent controverses), laugmentation asymptomatique
des concentrations sriques de troponine en postopratoire,
linfarctus du myocarde, linsuffisance cardiaque, larrt
cardiorespiratoire et jusquau dcs. Globalement, les complications graves concernent 3% des chirurgies et la mortalit globale
postopratoire est estime 0,5% [3].
Dans beaucoup de recommandations concernant lvaluation
propratoire des patients ayant une cardiopathie [5, 6, 7], le
risque de complications cardiovasculaires en fonction du type de
chirurgie est class en faible, modr ou lev [6] (Tableau 40-I).
Plus en dtail, sur une cohorte de 3,7millions de patients, la mortalit postopratoire (ajuste sur les comorbidits propratoires)
tait en moyenne de 1,85% mais avec une dispersion allant, sur
Tableau 40-I Risque de complications cardiovasculaires postopratoires
en fonction du type de chirurgie, daprs [5, 6, 7].
Risque de complications cardiovasculaires en fonction du type de chirurgie
lev
Incidence des complications > 5 %

Interventions chirurgicales majeures, en urgence,
surtout chez les patients gs
Chirurgie aortique ou vasculaire majeure
Chirurgie vasculaire priphrique
Interventions chirurgicales avec variations
importantes de volmie
Intermdiaire
Incidence des complications < 5 %

Endartriectomie carotidienne
Chirurgie tte et cou
Chirurgie intrapritonale et intrathoracique
Chirurgie orthopdique
Chirurgie prostatique
Faible
Incidence des complications < 1 %

Procdures endoscopiques
Chirurgie superficielle
Cataracte
Chirurgie du sein
218
ANESTH S IE
11catgories de chirurgies, de 0,07% (chirurgie du sein) 5,9%

(chirurgie vasculaire) [8]. Lorsque 37 procdures chirurgicales
ont t analyses, le risque de mortalit le plus lev (entre 15 et
20%) tait associ la transplantation pulmonaire ou hpatique
[8]. Ces rsultats suggrent que la classification du risque chirurgical en faible, modr et lev est une simplification, mais nanmoins acceptable car laire sous la courbe ROC (receiver operating
characteristic) de la classification complexe est de 0,88 alors que
celle de la classification simplifie est quand mme de 0,83, ce qui
est acceptable pour la pratique quotidienne.
Il faut souligner que pour le mme type de chirurgie, les vnements/complications peropratoires ne sont pas pris en considration [8]. Un score (score Apgar chirurgical) (Tableau 40-II)
prenant en compte les pertes sanguines peropratoires estimes,
les valeurs les plus basses de pression artrielle et de frquence cardiaque pendant la chirurgie, permet de stratifier le risque chirurgical en fonction dvnements peropratoires [9]. Il a t montr
que mme aprs ajustement sur 27variables propratoires, le score
Apgar chirurgical est discriminant dans plusieurs types de chirurgies en mono- ou multicentrique. La mortalit et les complications
30jours taient de 7,9% et 33% respectivement lorsque le score
Apgar chirurgical tait entre 0-4 et de 0,5% et 3% respectivement
pour un score de 10 [9]. Sur la cohorte initiale, la valeur mdiane du
score tait de 7 ce qui tait associ une mortalit de 1,1% et une
frquence des complications de 9,1% [9]. Lavantage thorique de
la prise en compte simultane du risque a priori (voir Tableau 40-I)
et a posteriori (voir Tableau40-II) est une classification globale du
risque pouvant aboutir des modifications de la prise en charge en
fin dintervention (parcours patients spcifiques pour les patients
dfinis comme risque) mais cette dmarche na pas encore fait
lobjet dtudes prospectives.
Lensemble de ces donnes pidmiologiques suggre que
linteraction entre une prvalence leve des cardiopathies et
un nombre lev et croissant dinterventions chirurgicales invasives, dans les pays dvelopps, peut aboutir un nombre lev
de patients ayant une cardiopathie devant bnficier dune intervention chirurgicale et qui ncessitent une attention particulire.
Donnes pidmiologiques historiques

du risque li au patient
Historiquement, un antcdent de cardiopathie (risque li au
patient) augmentait le risque de complications cardiovasculaires
pri-opratoires mais une interaction existe entre le risque li au
patient et le risque li la chirurgie; mme si le risque patient est
lev, lincidence des complications cardiovasculaires graves est
faible pour les chirurgies faible risque. Ceci a abouti au fait que
lACC/AHA (American college of cardiology/American heart association) [6], lESC (European society of cardiology) [7] et la Sfar/
SFC (Socit franaise danesthsie et de ranimation/Socit
franaise de cardiologie) [5] recommandent lutilisation du score
de Lee (Tableau 40-III) [10] pour la stratification du risque de
complications cardiovasculaires pri-opratoires. Dans le score de
Lee initial [10] publi en 1999, la prsence dune insuffisance cardiaque ou dune coronaropathie (quelles quen soient les manifestations cliniques de ces deux types de cardiopathies) augmentait
le risque de survenue de complications cardiovasculaires pri-opratoires [10]. Les autres cardiopathies ntaient pas mentionnes,
probablement parce que le nombre de patients dans la cohorte de
dveloppement et de validation du score de Lee ntait pas suffisant. La discrimination et la calibration du score de Lee, qui a t
adopt par les recommandations Sfar/SFC de 2011 [5] ont t
analyses dans une revue systmatique [11]. Il a t montr que la
discrimination tait acceptable (aire sous la courbe ROC de 0,75)
pour la chirurgie non vasculaire et mdiocre pour la chirurgie vasculaire (aire sous la courbe ROC 0,69). Les auteurs de la revue
systmatique [11] concluaient quil tait nanmoins raisonnable
dutiliser le score de Lee pour la stratification du risque cardiovasculaire pri-opratoire. La performance mdiocre du score de Lee
chez les patients de chirurgie vasculaire pourrait tre amliore par
lutilisation des biomarqueurs comme le peptide natriurtique de
type B [12] ou lchocardiographie de dpistage [13] mais la Sfar/
SFC en 2011 na pas fait de recommandations dans ce sens [5]. En
attendant la validation de scores de prdiction plus labors [14]
dont le calcul sera facilit par lutilisation des dossiers mdicaux
lectroniques, le score de Lee, de par sa simplicit dutilisation et
ses performances discriminatives acceptables, permettra au moins
dhomogniser les pratiques danesthsie et cest probablement
la principale raison pour laquelle il a t adopt par les socits
savantes dont la Sfar/SFC.
Donnes pidmiologiques rcentes

concernant le risque li au patient
Dans la publication qui a analys le plus grand nombre de patients
(183069) qui ont bnfici dune chirurgie non cardiaque [15],
les complications analyses ont t larrt cardiaque et linfarctus du myocarde (IDM) dans les trente jours postopratoires.
Tableau 40-II
Score Apgar chirurgical, daprs [9].

0 point
1 point
2 points
3 points
Pertes sanguines
estimes (mL)
>1000
601-1000
101-600
< 100
PAM la plus
basse (mmHg)
<40
40-54
55-69
>70
Frquence
cardiaque la
plus basse (bpm)
>85
76-85
66-75
56-65
4 points
<55
bpm : battements par minute ; PAM : pression artrielle moyenne.

La survenue dune brady-arythmie, incluant un bloc sinusal, un bloc auriculo-ventriculaire
ou un rythme dchappement jonctionnel ou ventriculaire, une asystolie est galement
cote comme 0.
Tableau 40-III Score de risque de complications cardiovasculaires

pri-opratoires (score de Lee) en fonction des caractristiques
propratoires et du type dintervention, daprs [10].
Chirurgie risque
1 point
Coronaropathie
1 point
Insuffisance cardiaque
1 point
Antcdents daccident vasculaire crbral
1 point
Diabte insulino-dpendant
1 point
Cratininmie > 2 mg . dL1
1 point
Chaque item correspond (hormis la chirurgie) une pathologie existante ou un

antcdent. La valeur de cratininmie est celle mesure lors de la consultation.
A N E STH SI E D U C A R D I AQ U E P O U R C H I R U R G I E N O N C A RD IAQ UE
Lincidence de ces complications cardiovasculaires graves tait de

1,29% (soit 2362 sur 183069 patients) mais avec une mortalit
trente jours de 60% [15]. Pour comparaison, lincidence des complications respiratoires tait de 3% [16] et celle des complications
thromboemboliques de 0,63% avec une mortalit trente jours
de 11 % [17]. Si dautres complications cardiovasculaires priopratoires sont prises en compte (par exemple linsuffisance cardiaque aigu, les troubles du rythme dont la fibrillation atrialeet
les accidents vasculaires crbraux), leur frquence augmente.
Ces rsultats dmontrent que les complications cardiovasculaires
graves sont moins frquentes que dautres types de complications
mais leur survenue est accompagne dune mortalit trs leve.
Mme lorsquelles nentranent pas le dcs en postopratoire
immdiat, les complications cardiovasculaires augmentent la
dure de sjour, les dpenses de sant et sont probablement responsables dune diminution de la survie distance.
Laccumulation des tudes de cohorte, sur un nombre de plus
en plus important de patients qui permet lajustement sur de plus
nombreuses variables propratoires, modifie lpidmiologie des
complications cardiovasculaires pri-opratoires chez les patients
ayant une cardiopathie. Dans ltude de Davenport et al. publie
en 2007 [15], en analyse multivarie, la prsence de plusieurs
types de cardiopathies (Tableau 40-IV) ntait pas statistiquement associe la survenue de complications pri-opratoires. Les
facteurs statistiquement associs un risque accru de survenue de
complications cardiovasculaires graves taient le type de chirurgie
et le statut fonctionnel ASA (American society of anesthesiologists)
[15]. Les auteurs concluaient que les antcdents de cardiopathie diagnostique et traite ne sont pas associs la survenue
des complications cardiovasculaires graves pri-opratoires. Ces
affirmations sont probablement acceptables pour la cardiopathie
ischmique car elle a t analyse en tenant compte de son histoire naturelle (angor, IDM, revascularisation coronaire). Ceci est
aussi probablement vrai en ce qui concerne lhypertension artrielle traite. Il faut souligner que les valvulopathies navaient pas
t identifies (autrement que par leur volution vers une insuffisance cardiaque) [15]. Dautres cardiopathies (hypertension artrielle pulmonaire ou HTAP, cardiomyopathies hypertrophiques
obstructives ou CMO) navaient pas t analyses non plus.
Ltude de Davenport et al. [15] a le mrite davoir la puissance statistique ncessaire pour retrouver (ou infirmer) une
association statistique entre les antcdents de cardiopathie et la
survenue de complications cardiovasculaires graves pri-opratoires mais ne rpond pas aux proccupations quotidiennes des
Tableau 40-IV Types de cardiopathies propratoires qui ntaient

pas statistiquement associes un risque accru de complications
postopratoires, daprs [15].
Insuffisance cardiaque congestive
Angor deffort
Infarctus du myocarde
Hypertension artrielle traite
Angioplastie coronaire
Chirurgie cardiaque avant la chirurgie non cardiaque
Artriopathie des membres infrieurs
219
praticiens lorsquil faut prendre en charge un patient donn avec

une cardiopathie et ses traitements. Il semble donc important
danalyser galement la littrature partir de cardiopathies plus
rares et mieux dfinies mais dans des tudes avec un nombre de
patients beaucoup plus faible. Cette analyse non exhaustive de la
littrature est prsente dans le Tableau 40-V.
La difficult, en 2012 et dans les annes venir, est de concilier
dun ct les donnes historiques qui ont permis la formulation
des recommandations dutiliser le score de Lee pour la stratification du risque propratoire (dans un objectif dhomognisation
des pratiques) et les rsultats plus rcents, obtenus sur de grandes
cohortes de patients, qui ne montrent pas de relation statistique
entre les antcdents de cardiopathie et la survenue de complications graves pri-opratoires. Par exemple, historiquement,
une attention particulire a t porte aux coronaropathies et
beaucoup de recommandations, y compris rcentes, sur lvaluation propratoire et la prise en charge pri-opratoire ont surtout concern ces patients [5, 7]. De manire surprenante, des
travaux plus rcents [18] montrent que la mortalit postopratoire trente jours des patients ayant une coronaropathie diagnostique et traite (6,6%) est similaire celle de patients sans
coronaropathie documente (6,2%) alors que la prsence dune
insuffisance cardiaque, quelle quen soit ltiologie, est associe
une augmentation (11,7 %) statistiquement significative du
risque de mortalit. Ces rsultats ont t confirms par une autre
tude publie en 2011 [19] qui a montr que la mortalit trente
jours ajuste pour de nombreuses covariables tait 2-3 fois plus
importante pour les patients ayant une insuffisance cardiaque
ischmique ou non ischmique ou une fibrillation atriale par
rapport aux patients ayant une coronaropathie. Il existe plusieurs
explications possibles ces discordances : 1) beaucoup de cardiopathies (surtout ischmiques) sont infracliniques et labsence
dantcdents identifis de coronaropathie dans le score de Lee
nexclue pas lexistence dune coronaropathie pouvant dcompenser en pri-opratoire ; 2) beaucoup de cardiopathies sont
correctement traites et les soins pri-opratoires modernes ne les
dcompensent pas; 3) la prise en charge pri-opratoire (fonde
surtout sur des raisonnements physiopathologiques) est correcte
et permet de prvenir beaucoup de complications pri-opratoires; 4) enfin, de trs nombreux biais mthodologiques peuvent
contribuer expliquer ces diffrences : biais dchantillonnage
dans les tudes monocentriques ou multicentriques prospectives
qui ont exclu beaucoup de patients de la vie relle; cohortes
anciennes (comme celle du score de Lee) qui ne bnficiaient
pas des prises en charge modernes (mdicales et chirurgicales) ;
limperfection des outils statistiques avec surtout le nombre de
facteurs dajustement dans les analyses multivaries qui ont t
utilises pour dfinir les scores. Labsence de relation statistique
entre la prsence de certaines cardiopathies et les complications
cardiovasculaires graves pri-opratoires pourrait tre une incitation dplacer lattention et les efforts des cliniciens de la stratification exclusivement propratoire du risque vers une stratgie
stratification pr- (score de Lee) et peropratoire (score Apgar
chirurgical) associe une surveillance cible des patients identifis comme tant haut risque avec prvention et traitement
rapide peret surtout postopratoire des anomalies pouvant dstabiliser la cardiopathie (activation excessive du systme nerveux
sympathique par lhypovolmie, lhypoxmie, la douleur, linfection, etc.). Cette stratgie semble conforte par une tude publie
en 2010 [20] et sera dveloppe ultrieurement.
220
ANESTH S IE
Tableau 40-V Estimation du risque de complications cardiovasculaires pri-opratoires (chirurgie non cardiaque) en fonction du type de cardiopathie.
Nombre de
patients
Pathologie
Complications
analyses
Risque de complications
pri-opratoires
Remarques
Kertai et al.
2004 [90]
RA svre
et modr
108 RA versus
216 contrles
Mortalit priopratoire et IDM
Ajust
OR : 5,2 (IC 95 % : 1,6-17)
14% de complications dans le groupe

RA versus 2% de complications dans le
groupe contrle
Calejja AM
et al. [91]
RA svre
asymptomatique
30
Dcs, IDM, ICC,

TDRV, hTAIO
Complications: 33% RA versus

23% contrle, P=0,06
Ho et al. [92]
RA modr
asymptomatique
22
Cardiovasculaires,
rnales
Pas de complications
Anesthsie pridurale; chirurgie

orthopdique
Zahid et al.
[93]
RA
5149 RA versus
10284 contrles
Ajust :
IDM : OR : 1,55 (IC 95%: 1,271,90), P<0,001
Mortalit pri-opratoire: NS
Analyse rtrospective, base de donnes

(National hospital discharge survey)
Torsher et al.
[31]
RA svre
symptomatique
19
Non spcifi
2 dcs
Analyse rtrospective
OKeefe et al.
[94]
RA svre
48
Non spcifi
0 dcs
Pour 7 patients complications dont
6 sans consquences
Raymer et al.
[95]
RA svre
55 RA versus
55 contrles
Dcs, IDM, ICC, TDR,

sjour prolong en
ranimation pour
problme cardiaque
Complications
N=5 dans RA
N=6 dans contrle
P=1
Hreybe et al.
[96]
CMO
227 CMO versus

554 contrles
Ajust
Dcs: 1,6 (IC 95 % : 1,46-1,77),
P<0,001
Dcs et IDM: 2,82
(IC 95% : 2,59-3,07), P<0,001
Analyse rtrospective, base de donnes

(National hospital discharge survey)
Hernandez
et al. [18]
Insuffisance
cardiaque
1532 patients
avec insuffisance
cardiaque
1757 patients avec
coronaropathie
Contrles : 44512
patients
Mortalit 30 jours
Radmission
lhpital
Ajustement sur type de chirurgie

Mortalit : 11,7% si insuffisance
cardiaque (P<0,001 versus les
autres); coronaropathie: 6,6%
(NS versus contrle); contrle
6,2%
Howell et al.
[97]
HTA
Complications
OR: 1,35 (IC95% : 1,17-1,56),

P<0,05
Mta-analyse de 30 tudes
observationnelles
Lai et al. [98]
IA modre
svre
167 patients
avec IA
et 167 contrles
Complications
cardiovasculaires,
dcs, instabilit
hmodynamique
peropratoire
Complications : 16,2% IA versus

5,4% contrle, P=0,003
Dcs : 9% IA versus
1,8% contrle, P=0,008
En analyse multivarie, la mortalit tait

significativement associe la prsence
dune IA grave, dune altration de la
fonction systolique ventriculaire gauche,
dune dysfonction rnale, dune chirurgie
risque et labsence de traitement
mdicamenteux
Lai et al. [99]
Insuffisance mitrale
svre modre
84 patients
Complications
cardiovasculaires,
dcs, instabilit
hmodynamique
peropratoire
31 % des patients ont fait des

complications hmodynamiques
mineures peranesthsiques
En postopratoire: 27% des
patients OAP ; 12% de mortalit
postopratoire
La survenue dune FA augmente le risque

de mortalit par un facteur 11
Le risque de complications postopratoires
est augment par une chirurgie risque
(facteur 5) et par la survenue dune FA
(facteur 3)
Lai et al. [100]
HTAP svre
62 patients
avec HTAP
et 62 contrles
Complications
cardiovasculaires,
dcs, instabilit
hmodynamique
peropratoire
ICA (9,7% HTAP versus 0%

contrle), P= 0,028
Intubation prolonge (21% HTAP
versus 3% contrle), P= 0,004
Dcs intrahospitalier (9,7% HTAP
versus 0% contrle), P= 0,028
En analyse multivarie, une chirurgie en

urgence (OR=44), une coronaropathie
(OR=9) et une HTAP (OR=1,1 ;
P<0,02) taient associes un risque
accru de mortalit postopratoire
Ramakrishna
et al. [101]
HTAP
145 patients
Dcs
7%
Les facteurs prdictifs de mortalit taient

les antcdents dembolie pulmonaire,
une dysfonction ventriculaire droite, un
rapport PAPS/PAS>0,66 et lutilisation
peropratoire dinotropes
CMO : cardiomyopathie hypertrophique obstructuve ; FA : fibrillation atriale ; hTAIO : hypotension artrielle intra-opratoire ; HTAP : hypertension artrielle pulmonaire ; IA : insuffisance
aortique ; IC : intervalle de confiance ; ICA : insuffisance cardiaque aigu ; ICC : insuffisance cardiaque chronique ; IDM: infarctus du myocarde; NS : non significative ; OAP : dme aigu du
poumon ; OR: odds ratio ; PAPS : pression artrielle pulmonaire systolique ; PAS : pression artrielle systolique ; RA: rtrcissement aortique ; TDRV: troubles du rythme ventriculaire.
Principes gnraux de prise

en charge pri-opratoire des
patients ayant une cardiopathie
La prise en charge pri-opratoire des patients ayant une cardiopathie a pour but principal de ne pas aggraver, voire damliorer,
lhistoire naturelle de la cardiopathie. Malgr des diffrences
importantes dans la physiopathologie, les manifestations cliniques et lhistoire naturelle des cardiopathies, il existe des principes gnraux pour la prise en charge pri-opratoire des patients
ayant une cardiopathie.
Les principales tapes de la prise en charge pri-opratoire sont:
1) lvaluation et la prise en charge propratoire avec la dcision
de pratiquer/reporter lacte anesthsique et les ajustements des
traitements chroniques; 2) le choix dune stratgie anesthsique
(choix du monitorage, de la technique danesthsie, des mdicaments anesthsiques, des modalits de maintien de lhomostasie) ; 3) le choix dune stratgie de surveillance postopratoire,
de prvention, diagnostic et traitement des complications et de
rinstitution des traitements chroniques propratoires.
Les principes de lvaluation propratoire des patients ayant
une cardiopathie et devant bnficier dune chirurgie non cardiaque ont t exposs dans les recommandations de lACC/
AHA en 2007 [6], de lESC en 2009 [7] et de la Sfar/SFC en 2011
[5]. Ces recommandations dfinissent comme buts: 1) didentifier les patients ayant une cardiopathie instable (Tableau40-VI)
devant, en dehors de lurgence chirurgicale vitale, bnficier dune
prise en charge spcialise avant lintervention de chirurgie non
cardiaque; 2) de crer, pour les patients ayant une cardiopathie
Tableau 40-VI Situations cliniques qui ncessitent une valuation/prise

en charge cardiologique avant une intervention rgle, daprs [5, 6, 7].
Situation clinique
Syndrome coronarien
aigu
Exemples
Angor instable ou angor svre (CCS classe III
ou IV)
Infarctus du myocarde rcent (entre 7 et 30 jours)
Insuffisance cardiaque
dcompense (NYHA
IV) ou insuffisance
cardiaque aigu
Troubles du rythme
ou de la conduction
Valvulopathies svres
Bloc auriculo-ventriculaire de haut degr (Mobitz

II, III)
Troubles du rythme ventriculaire symptomatiques
Arythmies supraventriculaires avec frquence
ventriculaire non contrle (frquence
cardiaque de repos>100bpm)
Bradycardie symptomatique
Tachycardie ventriculaire de diagnostic rcent
Rtrcissement aortique svre (gradient moyen
>40mmHg, surface aortique<1cm2 ou
symptomatique)
Stnose mitrale symptomatique (dyspne
daggravation progressive leffort, syncope
deffort ou insuffisance cardiaque) ou surface
<1,5cm2
CCS : Canadian cardiovascular society ; NYHA : New York heart association.
221
stable, un cadre de rflexion, de dfinir les meilleures approches

diagnostiques et thrapeutiques, de dmontrer que des interventions diagnostiques et thrapeutiques sont rarement ncessaires
pour faire passer le cap de lintervention chirurgicale et de
lanesthsie et de limiter la prescription dexamens complmentaires cardiologiques coteux ; 3) de formaliser la rflexion
pour une troisime catgorie de patients, les patients asymptomatiques, sans facteurs de risque de complications cardiovasculaires
pri-opratoires identifis par le score de Lee mais ayant dautres
facteurs de risque cardiovasculaires (hypercholestrolmie, hypertension artrielle, obsit). La Sfar/SFC a considr quen France,
la consultation danesthsie et lvaluation propratoire ralise
ce moment ne pouvaient pas servir dvaluation cardiovasculaire
chez les patients asymptomatiques [5].
En consultation danesthsie, linterrogatoire est centr sur
la recherche des facteurs de risque cardiovasculaires, des antcdents (hospitalisations pour dcompensation dune insuffisance
cardiaque, angor deffort, IDM, souffle cardiaque, palpitations,
artriopathie des membres infrieurs), des interventions diagnostiques ou thrapeutiques (coronarographie, revascularisation
coronaire, stimulateurs ou dfibrillateurs cardiaques), des traitements cardiovasculaires et des comorbidits. Lestimation de la
capacit leffort du patient en fonction dune chelle comme
celle de Duke (Tableau 40-VII) est une tape essentielle de lvaluation propratoire [5]. Dans le score de Duke, lactivit physique est exprime en METs (metabolic equivalents). Pour chaque
type dactivit physique, la dpense nergtique correspond un
certain nombre de METs. La capacit fonctionnelle est considre comme excellente (>7METs), modre (4-7METs), mauvaise (< 4 METs) ou inconnue. Les complications cardiaques
pri-opratoires surviennent plus frquemment chez les patients
dont les capacits fonctionnelles sont infrieures 4METs.
Linterrogatoire et lexamen clinique raliss lors de la consultation danesthsie ainsi que la connaissance du type de chirurgie
(voir Tableau 40-I) permettent de calculer le score de Lee (voir
Tableau 40-III) et de dfinir pour chaque patient un risque a
priori faible (moins de 1point), intermdiaire (1 ou 2points) ou
lev (3points ou plus). Les patients risque faible nont, en gnral, pas besoin dexplorations complmentaires [7]. Les patients
risque lev ncessitent souvent une optimisation du traitement,
habituellement ralise par les cardiologues [7]. Les examens complmentaires ventuels permettent, aprs analyse des rsultats, de
reclasser surtout les patients risque intermdiaire et daffiner
lestimation du risque [7].
Tableau 40-VII
chelle de Duke, daprs [5, 6, 7].
Besoins nergtiques estims selon le type dactivit physique

1 MET
Se prendre en charge soi-mme pour les activits

de la vie courante (repas, toilette)
Marcher dans la maison
Marcher dans la rue la vitesse de 3-5 km/h
4 METs
10 METs
Activits sportives importantes (natation, tennis en

simple, ski alpin)
Monter un tage sans sarrter

Marcher dans la rue la vitesse de 5-7 km/h
Activits domestiques importantes (laver par terre)
Activits sportives modres (danse, tennis en double)
222
ANESTH S IE
Prise en charge des patients

coronariens
Physiopathologie et prvention
des complications ischmiques myocardiques
pri-opratoires
La principale tiologie des coronaropathies est lathrome coronarien. Les manifestations cliniques de lathrome coronarien
peuvent prendre la forme de langor chronique stable en relation
avec des stnoses des artres coronaires qui empchent laugmentation du dbit sanguin coronaire (DSC) lors des augmentations
de la consommation en oxygne du myocarde (MvO2) ou bien
des syndromes coronariens aigus (SCA) dont lIDM pour lequel
existent des dfinitions internationales, applicables aussi au
contexte pri-opratoire (Tableau 40-VIII) [21].
Tableau 40-VIII Dfinitions internationales de linfarctus
du myocarde, daprs [102].
Le terme infarctus du myocarde (IDM) devrait tre utilis lorsquil existe une
augmentation de la troponine srique (au moins une valeurs suprieure
au 99e percentile de la limite haute de rfrence) AVEC au moins un des
lments suivants :
symptmes dischmie
signes ECG vocateurs dischmie (modifications du segment ST ou
apparition dun bloc de branche gauche)
apparition dune nouvelle onde Q
imagerie compatible avec une perte de novo de myocarde viable ou
lapparition de novo danomalies de la contractilit segmentaire
Le terme dIDM ne peut pas tre utilis pour dsigner les dommages
myocardiques associs la chirurgie cardiaque ni les dommages
myocardiaques secondaires des pathologies comme linsuffisance
rnale chronique, linsuffisance cardiaque chronique, la cardioversion, les
ablations des procdudes dlectrophysiologie, le sepsis, la myocardite, les
toxines cardiaques, les pathologies infiltratives
Type 1
IDM spontan en relation avec une ischmie myocardique secondaire un
vnement coronarien primaire (rosion de plaque et/ou rupture/fissure/
dissection)
Type 2
IDM secondaire soit une ischmie myocardique secondaire, soit une
augmentation de la demande myocardique en oxygne ou une
diminution de lapport myocardique en oxygne (spasme coronarien,
embolie coronaire, anmie, arythmie, hyper- ou hypotension artrielle)
Type 3
Mort subite, y compris arrt cardiaque, souvent avec des symptmes
suggrant une ischmie myocardique, accompagns par des anomalies
prsumes de novo comme un sus-dcalage du segment ST, un bloc de
branche gauche ou des preuves de lexistence dun thrombus coronaire
(angiographie et/ou autopsie). Le dcs survient avant le prlvement
dchantillons permettant de mesurer les enzymes cardiaques (ou le
prlvement est fait avant laugmentation des enzymes cardiaques)
Type 4a
IDM associ une angioplastie coronaire (laugmentation de la troponine
doit tre suprieure, par convention, trois fois la valeur du 99e percentile,
en cas de valeur normale de la troponine avant la procdure)
Type 4b
IDM associ une thrombose du stent documente en angiographie
ou lautopsie
Type 5
IDM survenant aprs un pontage aortocoronarien (laugmentation de la troponine
doit tre suprieure, par convention, cinq fois la valeur du 99e percentile)
IDM : infarctus du myocarde
Lischmie myocardique et les SCA pri-opratoires peuvent

tre conus comme le rsultat dune interaction complexe entre
lathrome coronarien prexistant et des causes extracardiaques
qui le dstabilisent en pri-opratoire (Tableau 40-IX). partir de ces concepts physiopathologiques, il existe deux stratgies
qui ne sexcluent pas mais qui ont polaris lattention des cliniciens et sont refltes dans la littrature. La premire est centre sur le dpistage et la correction propratoire de lathrome
svre aboutissant des stnoses coronariennes stables (pouvant
justifier dune revascularisation myocardique) avec lespoir de
faire passer le cap de lintervention. Il nexiste pas de preuves
convaincantes que cette stratgie coteuse diminue la morbidit
et la mortalit pri-opratoires. Les recommandations Sfar/SFC
de 2011 [5] stipulent que la dcision de revascularisation myocardique avant une chirurgie non cardiaque doit tre collgiale et
trace dans le dossier mdical (bnfices/risques/alternatives avec
optimisation du traitement mdical) et clairement explique au
patient; elle doit rester une dcision exceptionnelle fonde soit
sur la survenue dun SCA (avec ou sans sus-dcalage du segment
ST), soit sur lexistence dune coronaropathie stable avec statut
anatomique particulier (stnose du tronc commun coronaire
gauche ou des trois troncs coronaires ou pluritronculaire impliquant lartre interventriculaire antrieure). La technique de rfrence pour la revascularisation avant une chirurgie non cardiaque
est le pontage coronarien en cas de stnose du tronc commun.
Si une angioplastie coronaire est choisie, elle doit faire appel aux
prothses endocoronaires nues cause des dlais de seulement six
semaines avant de pouvoir pratiquer une chirurgie non cardiaque.
La deuxime stratgie est centre sur la prvention de la survenue
des situations qui risquent de dstabiliser lathrome coronarien
(tachycardie, hypothermie, anmie, hypoxmie, douleur) en activant le systme sympathique ainsi que sur la prvention mdicamenteuse des consquences de lactivation sympathique excessive.
Tableau 40-IX Dterminants de la balance apport/demande

myocardique en oxygne.
Diminution de lapport en oxygne
au niveau myocardique
Diminution de la pression
de perfusion coronarienne
Diminution du contenu artriel
en oxygne
Vasospasme coronarien
Augmentation de la demande
en oxygne myocardique
Augmentation de la frquence
cardiaque
Augmentation de la prou postcharge ventriculaire
Augmentation de la contractilit
Situation clinique associe

Hypotension artrielle
Anmie
Anomalies de la vasomotricit
coronarienne sur athrome
prexistant
Situation clinique associe

Troubles hmodynamiques
(hypovolmie) ou anesthsie
insuffisante
Troubles hmodynamiques
(surcharge volmique)
ou anesthsie insuffisante
Inotropes ou niveau danesthsie
inadquat
valuation propratoire des patients ayant

une coronaropathie
Au terme de lvaluation propratoire ralise selon les principes gnraux dcrits prcdemment, lalgorithme dcisionnel
(Figure40-1) de la Sfar/SFC [5], simplifi par rapport aux prcdentes recommandations internationales [7], permet de rpondre
aux questions pratiques (faut-il reporter lanesthsie ? ; faut-il
adresser le patient un cardiologue?) poses lors de la consultation danesthsie propratoire. la fin de lvaluation clinique
propratoire, en utilisant des critres cliniques simples et en
connaissant le risque li au type dintervention, trois types dattitudes peuvent tre adoptes: 1) le patient doit bnficier dune
chirurgie pour laquelle le risque de complications cardiovasculaires peropratoires est faible (< 1 %). Les recommandations
ACC/AHA, ESC et Sfar/SFC [5, 6, 7] stipulent que les examens
complmentaires et la consultation de cardiologie ne sont pas
utiles, surtout lorsque la cardiopathie est stable. Le mdecin anesthsiste-ranimateur peut nanmoins obtenir de la part du cardiologue lensemble du dossier mdical du patient; 2) le patient
a une cardiopathie dont la gravit, la stabilit et la thrapeutique
sont documentes, est suivi par un cardiologue et doit bnficier
dune chirurgie risque leve. Dans cette situation, le patient est
class comme tant haut risque et le principal souci doit tre
non pas les examens complmentaires cardiologiques mais loptimisation du traitement. Le mdecin anesthsiste-ranimateur et
le cardiologue doivent dcider si le patient peut bnficier dun
223
traitement curatif cause de lvolution ou de la gravit de la cardiopathie (exemple: revascularisation coronarienne ou chirurgie
valvulaire), indpendamment de lintervention pour laquelle le
patient est adress. Le message important des recommandations
[5, 6, 7] est que la correction ventuelle (avant la chirurgie non
cardiaque) de la cardiopathie doit tre indique sur sa gravit et
non sur la ncessit de protger le patient pour lui faire passer
le cap de lintervention. Lorsque la cardiopathie nest pas suffisamment volue pour justifier une correction spcifique, il faut
sassurer que le traitement mdical est optimal, conformment
aux recommandations pour les diffrents types de cardiopathies.
Il a t montr que plus de 30% des patients pouvaient bnficier dune optimisation propratoire de leur traitement mdical
(prescription de nouveaux mdicaments cardiovasculaires ou
optimisation des doses) [13] ; 3) le patient a plusieurs facteurs
de risque de maladies cardiovasculaires, la cardiopathie nest
pas connue, la capacit leffort du patient ne peut pas tre value (atteinte vasculaire priphrique par exemple) et le patient
doit bnficier dune intervention chirurgicale risque lev ou
intermdiaire. Dans cette situation, les explorations complmentaires ralises par le cardiologue peuvent permettre soit de
classer le patient comme tant faible risque, soit au contraire
comme tant risque lev auquel cas loptimisation du traitement doit tre envisage. Ce problme concerne surtout lidentification des patients ayant une atteinte coronarienne pauci- ou
asymptomatique.
Figure 40-1 Algorithme de prise en charge propratoire des patients ayant une cardiopathie et devant bnficier dune intervention ncessitant une
anesthsie propos par la Socit franaise danesthsie et de ranimation et par la Socit franaise de cardiologie, daprs [5].
224
ANESTH S IE
Rle de la consultation de cardiologie

et des examens complmentaires
dans lvaluation anesthsique
avant une chirurgie non cardiaque
Le choix des examens complmentaires pour affiner lestimation

du risque cardiaque pri-opratoire est du ressort du cardiologue.
La Sfar/SFC a fait [5] des recommandations concernant la prescription dexamens complmentaires pour dtecter une ischmie
myocardique avant une intervention. Les examens complmentaires le plus frquemment prescrits sont lECG de repos, lchocardiographie de repos, lECG ambulatoire, lECG deffort, la
scintigraphie myocardique deffort ou sensibilise (dipyridamole
ou dobutamine), lchocardiographie deffort ou sensibilise
(dobutamine avec ou sans atropine). Pour la pratique quotidienne,
la Sfar/SFC a restreint les indications de lECG de dbrouillage
[5, 22] (Tableau 40-X); la prescription dun ECG de repos nest
pas recommande, quel que soit lge du patient, en cas: 1) dintervention faible risque chirurgical; 2) quel que soit le risque li la
chirurgie, si un ECG est disponible depuis moins dun an et en labsence de modifications cliniques [22]. La Sfar/SFC a svrement
restreint la prescription de lchocardiographie de repos de dpistage chez les patients asymptomatiques avec une possible exception
(mais non valide) pour la chirurgie vasculaire o il a t montr,
dans une tude [23], que la prsence dune dysfonction systolique ou diastolique chocardiographique, asymptomatiques, tait
un facteur de risque indpendant de survenue de complications
cardiovasculaires aprs chirurgie vasculaire ciel ouvert mais pas
aprs chirurgie vasculaire endoluminale [23]. En ce qui concerne
les autres examens cardiologiques spcialiss, les recommandations
Sfar/SFC laissent les cardiologues dfinir et interprter les examens
Tableau 40-X Indications de llectrocardiogramme propratoire de
dpistage, daprs [5].
appropris pour diagnostiquer une coronaropathie infraclinique

[5, 6, 7]. Il faut nanmoins que les mdecins anesthsistes-ranimateurs connaissent la sensibilit, la spcificit et les valeurs prdictives positives et ngatives de ces examens complmentaires pour
la prdiction des complications cardiovasculaires postopratoires
(Tableau 40-XI). De manire gnrale, les valeurs prdictives ngatives sont leves et les valeurs prdictives positives (trs) faibles.
Une fiche de liaison a t propose en 2011 dans les recommandations Sfar/SFC [5] (Figure40-2).
tiquette du patient : ...........................................................................................
Coordonnes du patient : .....................................................................................
Date de demande : ...............................................................................................
Nom et tlphone de lanesthsiste : ...................................................................
Antcdents cardiaques connus (prciser et joindre les comptes rendus,
cardiologue traitant) :
UCoronaires : ......................................................................................................
U Autres : RA, autres valves, HTA, FA, antcdents vasculaires
Prsence dun stent coronaire : Oui U Non U
Si oui, dtails (type, date, actif ?, correspondant) : ................................................
Interrogatoire :
Angor : Non U Oui U Possible U
Dyspne : Non U Oui U
Stade NYHA : 1 2 3 4
Capacit leffort : (le patient peut-il monter 2 tages?)
Examen clinique : FC TA
Autre information utile : ........................................................................................
ECG ( joindre) : ....................................................................................................
Type dintervention programme : ...................... Date prvue : ...........................
Chirurgie risque : lev U intermdiaire U faible U
Motif de lintervention (oncologie, hmorragie, menace vitale, fracture,
fonctionnelle, etc.) : ..........................................................................................
La chirurgie peut-elle tre repousse ? : Oui U Non U
Traitement actuel (dont antiagrgants, btabloquant, mdicaments de lIC,
statines) : ......................................................................................................
Si traitement par antiplaquettaire, la chirurgie peut-elle tre ralise sous
aspirine et/ou clopidogrel?
Score de risque ( remplir par lanesthsiste) : ......................................................
Risque patient/risque
chirurgical
Faible
Intermdiaire
Majeur
Faible
Intermdiaire
Majeur
Non
Non
discuter
discuter
discuter
Oui
Oui
Oui
Oui
Pour les patients gs de plus de 65 ans, il faut probablement prescrire un ECG12 drivations
de repos avant toute intervention risque intermdiaire ou lev, mme en labsence de
signes cliniques, de facteurs de risque ou de pathologies cardiovasculaires [22].
Tableau 40-XI Performances diagnostiques des principaux examens

complmentaires de cardiologie pour la prdiction des complications
cardiovasculaires pri-opratoires, daprs [5, 6, 7].
Sensibilit
(%)
Spcificit
(%)
VPP
(%)
VPN
(%)
ECG deffort
74
69
10
98
Thallium avec
dipyridamole
83
47
11
97
chocardiographie
de stress (effort,
dobutamine,
dipyridamole)
85
70
25-45
90-100
Type de test
ECG: lectrocardiogramme; VPN: valeur prdictive ngative ; VPP: valeur prdictive positive.
Score de Lee :
Chirurgie haut risque U
U Cardiopathie ischmique
U ATCD AVC/AIT
U Diabte
U ATCD IC congestive
U Insuffisance rnale
Total :
Motif spcifique de la demande : ..........................................................................

CONSULTATION DE CARDIOLOGIE (joindre le compte rendu)
Nom du cardiologue : ............................................................................................
Coordonnes du cardiologue : ..............................................................................
Date de consultation : ...........................................................................................
Des examens ont-ils t raliss en consultation ?
Des examens complmentaires sont-ils recommands ?
ECG deffort : ........................................................................................................
Scintigraphie myocardique : ..................................................................................
chographie sous dobutamine : ............................................................................
Coronarographie : .................................................................................................
Autres : .................................................................................................................
Prvoir le dosage de la troponine I postopratoire : Oui U Non U
Recommandations thrapeutiques :
Btabloquants : .....................................................................................................
Statines : ...............................................................................................................
Anti-agrgants plaquettaires : ...............................................................................
Autres : .................................................................................................................
Figure 40-2 Exemple de fiche de liaison entre lquipe danesthsieranimation et lquipe de cardiologie (propose par la Socit franaise
danesthsie et de ranimation et par la Socit franaise de cardiologie,
daprs [5]).
Prophylaxie mdicamenteuse des complications

ischmiques pri-opratoires
Une des approches utilises pour tenter de diminuer lincidence

des pisodes dischmie myocardique pri-opratoires et de ses
consquences a t ladministration titre prophylactique de
mdicaments connus pour leurs effets anti-ischmiques myocardiques (les btabloquants) ou de stabilisation des plaques
dathrome (les statines). Les principales classes de mdicaments
utiliss dans cette indication sont les antagonistes des rcepteurs
bta-adrnergiques (`-bloquants), les agonistes _2-adrnergiques
(clonidine, dexmdtomidine, mivazrol), les drivs nitrs, les
antagonistes des canaux calciques et les statines.
Les effets cliniques des diffrentes classes thrapeutiques utilises dans la prvention de lischmie myocardique pri-opratoire
sont prsents dans le Tableau 40-XII.
Depuis la prcdente dition de ce livre qui dans ce chapitre
recommandait lutilisation prophylactique des `-bloquants chez
les patients risque de dvelopper une ischmie myocardique
pri-opratoire, ltude Poise [24] et plusieurs mta-analyses
[25, 26] ont montr que ladministration pri-opratoire prophylactique des `-bloquants diminuait de manire significative
lincidence des complications ischmiques myocardiques priopratoires mais augmentait ou ne modifiait pas la mortalit
globale, probablement en relation avec une incidence accrue des
accidents vasculaires crbraux, une hypotension artrielle et une
bradycardie pri-opratoires. Les recommandations actuelles
de la Sfar/SFC concernant la prophylaxie mdicamenteuse des
complications ischmiques pri-opratoires sont rsumes dans
le Tableau 40-XIII [5]. Ces recommandations soulvent le problme de la dure minimale propratoire de prophylaxie mdicamenteuse qui a un effet bnfique dmontr sur la diminution
des complications cardiovasculaires pri-opratoires. Une tude
suggre que le dlais minimum entre le dbut de la prescription
des `-bloquants et lintervention chirurgicale, associ avec un
effet bnfique sur la diminution de lincidence des complications
cardiovasculaire postopratoires, est de 7 jours [27].
Tableau 40-XII Mcanismes daction et effets cliniques des

principaux mdicaments utiliss dans la prophylaxie des complications
cardiovasculaires pri-opratoires, daprs [5, 6, 7].
Diminution
des pisodes
dischmie
myocardique
Diminution
des autres
complications
cardiovasculaires
graves
Diminution
de la
mortalit
Antagonistes
`-adrnergiques
Oui
Non
Non
Agonistes
_2-adrnergiques
Oui
Donnes
insuffisantes
Donnes
insuffisantes
Drivs nitrs
Oui
Non
Non
Antagonistes
calciques
Oui
Non
Non
Statines
Oui
Oui
Oui
225
Tableau 40-XIII Recommandations de la Sfar/SFC concernant la

gestion pri-opratoire des mdicaments cardiotropes chez les patients
ayant une coronaropathie, daprs [5].
Btabloquants
GRADE 1+
Continuer dans la priode pri-opratoire un traitement `-bloquant lorsquil
est prescrit pour une insuffisance coronaire, associe ou non un
antcdent de troubles du rythme ou une insuffisance cardiaque
Mettre en route en propratoire un traitement `-bloquant est recommand
chez les patients ayant une insuffisance coronaire clinique ou des signes
dischmie myocardique sur un examen non invasif
Utiliser pour une premire prescription un agent cardioslectif sans activit
sympathique intrinsque. Le dbut dun traitement de novo en propratoire
par un `-bloquant doit tre ralis entre 7-30 jours avant la date prvue
pour la chirurgie et la dernire prise avant lopration est le matin de
la chirurgie. Les doses doivent tre titres pour obtenir une frquence
cardiaque entre 60-80bpm tout en vitant une hypotension artrielle. Le
risque de bradycardie et dhypotension artrielle pri-opratoire doit tre
gr par le monitorage et la correction approprie de ces deux types de
complications
GRADE 2+
Chez les patients stratifis risque cardiovasculaire lev ou intermdiaire,
estim par un score de Lee clinique (hors facteur li la chirurgie) suprieur
ou gal 2, il peut tre recommand de dbuter un traitement `-bloquant
si le patient est opr de chirurgie haut risque. Lindication doit tenir
compte du risque li lhypotension et aux bradycardies peropratoires
GRADE 1Il nest pas recommand de dbuter un traitement `-bloquant si le patient est
opr de chirurgie faible risque, ni sil est faible risque
Agonistes alpha 2-adrnergiques

GRADE 2Les agonistes alpha 2-adrnergiques (clonidine, dexmdtomidine et mivazrol) ne
sont pas recommands pour la prophylaxie des complications cardiovasculaires
pri-opratoires en raison de leur retentissement hmodynamique
Statines
GRADE 1+
Un traitement par statine doit tre poursuivi dans la priode pri-opratoire
lorsquil est prescrit de faon chronique. Celui-ci doit tre administr le soir
prcdant lintervention et repris le soir de lintervention
Si un traitement par statine est indiqu, mais non prescrit au patient, il est
recommand de le dbuter avant une chirurgie vasculaire, si possible au
moins une semaine auparavant
GRADE 2+
Les patients devant subir une chirurgie vasculaire artrielle pourraient
bnficier de lintroduction dun traitement par statine, si possible au moins
une semaine auparavant
Inhibiteurs de lenzyme de conversion (IEC)

et antagonistes des rcepteurs de langiotensine 2 (ARA2)
GRADE 1+
Chez les patients coronariens, il est recommand de maintenir les IEC ou les
ARA2 dans la priode pri-opratoire, lorsque ceux-ci sont prescrits dans
le cadre dune insuffisance cardiaque et de tenir compte du risque accru
dhypotension artrielle pri-opratoire
Il est recommand dinterrompre un IEC ou un ARA2 au moins 12 heures
avant une intervention lorsque ceux-ci constituent un traitement de fond de
lhypertension artrielle
Antagonistes calciques et drivs nitrs

GRADE 1Ces deux classes de mdicaments ne sont pas recommandes pour la
prophylaxie des complications ischmiques priopratoires
GRADE dsigne: grades of recommendations, assessment, development, and evaluation
[103]. GRADE 1+ : il faut faire ; GRADE 1- : il ne faut pas faire ; GRADE 2+ ; il faut
probablement faire ; GRADE 2- : il ne faut probablement pas faire.
226
ANESTH S IE
Gestion pri-opratoire des traitements

par agents antiplaquettaires
La majorit des patients ayant une coronaropathie reoivent des

agents antiplaquettaires (AAP). La gestion pri-opratoire des
AAP a fait lobjet des recommandations publies en 2012 [28]
qui figurent dans les Tableaux 40-XIV et 40-XV.
Tableau 40-XIV Recommandations pour la gestion pri-opratoire

des agents antiplaquettaires, daprs [5, 38].
Traitement des pisodes dischmie

myocardique pri-opratoire
Le traitement de lischmie myocardique pri-opratoire doit

dabord tre tiologique. Les facteurs responsables de la balance
entre demande/apport en oxygne au niveau myocardique sont
reprsents dans le Tableau 40-IX. Un algorithme de traitement
des pisodes dischmie myocardique en fonction des diffrents
facteurs tiologiques est propos dans la Figure 40-3.
Prise en charge pri-opratoire

des patients ayant une valvulopathie
Des problmes communs la majorit des patients ayant une
valvulopathie concernent la connaissance de la physiopathologie
de la valvulopathie, lvaluation propratoire, la prophylaxie de
lendocardite bactrienne, dont les indications ont t restreintes,
et la gestion du traitement anticoagulant chez les patients qui ont
des indications danticoagulation au long cours. Le problme de
Tableau 40-XV
la gestion du traitement anticoagulant chronique est similaire

pour les patients ayant une indication danticoagulation pour
une fibrillation atriale (ou un flutter atrial) ou une pathologie
thromboembolique veineuse.
Chez les patients recevant de laspirine pour la prvention secondaire des

pathologies cardiovasculaires et devant bnficier de soins dentaires
mineurs ou de chirurgie superficielle ou de chirurgie pour cataracte, il est
recommand de continuer le traitement par aspirine
Chez les patients recevant de laspirine pour la prvention secondaire et
risque lev ou modr de complications postopratoires et devant
bnficier dune chirurgie non cardiaque, il est recommand de continuer
le traitement par aspirine
Linterruption du traitement par aspirine, 7-10 jours avant lintervention,
est recommand chez les patients faible risque de complications
cardiovasculaires postopratoires
Chez les patients porteurs de stents coronariens et recevant un traitement
par aspirine et clopidogrel et devant bnficier dune chirurgie non
cardiaque, il est recommand de reporter la chirurgie rgle pour une
priode de 6 semaines en cas de stent nu et de 6 mois en cas de stent
pharmacologiquement actif
En cas de chirurgie qui doit avoir lieu pendant les 6 semaines (stents nus) ou
6 mois (stents actifs), il est recommand de continuer le traitement par
aspirine et clopidogrel
Prise en charge pratique du traitement pri-opratoire par agents antiplaquettaires, daprs [5, 38].
Traitement propratoire
Quoi faire
Exception
Comment grer lexception
Type de chirurgie
Mineure
Majeure
Continuer AAP
Prvention primaire avec aspirine
ou clopidogrel
Arrter aspirine ou clopidogrel

5-7 jours avant lintervention
sans relais par HBPM ou HNF
Prvention secondaire par

aspirine ou clopidogrel
Continuer aspirine ou clopidogrel

Ne pas prescrire de
prophylaxie de la maladie
thromboembolique
postopratoire par HBPM
ou anticoagulants oraux
En cas de chirurgie dans un

espace ferm (neurochirurgie,
chirurgie mdulaire, chambre
postrieure de lil)
Arrter aspirine ou clopidogrel

5-7 jours avant lintervention
programme
Rintroduction de laspirine ou
du clopidogrel le lendemain
de la chirurgie en labsence de
contre-indication
Aspirine et clopidogrel chez les

patients haut risque
1. Reporter la chirurgie rgle

jusqu ce que le traitement
par les deux agents
antiplaquettaires ne soit plus
ncessaire
2. En cas de chirurgie semiurgente, continuer laspirine
avec ou sans clopidogrel
au cas par cas
3. En cas de chirurgie urgente,
continuer les deux agents
antiplaquettaires. Ne pas
prescrire de prophylaxie de
la maladie thromboembolique
postopratoire par HBPM
ou anticoagulants oraux
En cas de chirurgie dans une

cavit ferme (neurochirurgie,
chirurgie mdulaire, chambre
postrieure de lil)
Continuer laspirine et arrter

le clopidogrel 5 jours avant
lintervention programme
Considrer lutilisation dun AAP
type anti IIb/IIIa de courte
dure daction
Chez certains patients envisager
galement larrt de laspirine
Rintroduire les deux AAP le
lendemain de la chirurgie en
labsence de contre-indications
AAP: agents antiplaquettaires; HBPM: hparine de bas poids molculaire; HNF: hparine non fractionne.
Figure 40-3
227
Algorithme de prise en charge dun pisode dischmie myocardique pri-opratoire.
Physiopathologie et histoire naturelle

des valvulopathies
La connaissance de la physiopathologie des valvulopathies, des

mcanismes adaptatifs mis en jeu par lanomalie valvulaire et de
son histoire naturelle permet de dfinir la stratgie dvaluation
propratoire, les objectifs thrapeutiques pri-opratoires pour
assurer la stabilit hmodynamique ainsi que la mise en route
dun traitement adapt en cas danomalies hmodynamiques survenues en pri-opratoire. Ces lments dinformation sont rsums dans le Tableau 40-XVI. Des lments de physiopathologie,
spcifiques chaque type de valvulopathies, permettent daffiner
le raisonnement mdical.
RTRCISSEMENT AORTIQUE (RA)
La surface valvulaire aortique normale est de 3-4 cm2. Un RA

devient hmodynamiquement significatif lorsque la surface valvulaire aortique est <1 cm2. Les RA sont classs en peu svres
(surface > 1,5 cm2), modrs (1 cm2 < surface < 1,5 cm2) et
svres (surface<1cm2) [29]. Une stnose critique correspond
une surface <0,4cm2 et un gradient systolique >50mmHg
en prsence dune fonction systolique du VG conserve. En labsence des symptmes, la mortalit du RA (hors contexte priopratoire) est faible [29]. Lorsque des symptmes (syncope,
angor deffort, insuffisance cardiaque) apparaissent, la survie est
de 50% un an [30]. Il est important de dpister (auscultation
cardiaque) les patients ayant des RA asymptomatiques lors de
la consultation danesthsie et dadresser systmatiquement ces
patients au cardiologue pour valuation clinique et chocardiographique afin de leur permettre de bnficier du traitement
optimum.
Mme en cas durgence, le diagnostic propratoire chographique du RA est souhaitable et ces patients doivent tre
considrs comme ayant un risque accru de complications cardiovasculaires pri-opratoires. Le risque de mortalit pri-opratoire (chirurgie non cardiaque) chez un patient ayant un RA
dpend de la gravit de la stnose avec une mortalit denviron
11% (2patients sur 19) dans une srie de 19patients (ge moyen
75ans), ayant un RA svre ou critique connu en propratoire,
une fonction systolique du VG conserve et ayant bnfici

dune chirurgie non cardiaque, rgle ou en urgence, sous anesthsie gnrale dans la majorit des cas [31]. Cette tude, bien
que rtrospective, est importante car ses rsultats peuvent tre
extrapols aux patients ayant un RA svre et devant bnficier
dune chirurgie en urgence. Les auteurs avaient fait appel pour la
majorit des patients une mesure invasive de la pression artrielle et corrig rapidement les anomalies hmodynamiques par
linjection de phnylphrine [31].
Des stnoses coronariennes asymptomatiques ont t rapportes chez les patients ayant un RA et le risque de complications
ischmiques myocardique pri-opratoires est important chez
ces patients. La survenue dune ischmie myocardique sous endocardique, mme en labsence de stnoses significatives des artres
picardiques, a t mise sur le compte de lhypertrophie ventriculaire gauche et des anomalies de la microcirculation coronarienne.
La diminution de la compliance ventriculaire gauche diminue la
tolrance lhypovolmie et la tachycardie et rend les patients
ayant un RA dpendants de la contraction auriculaire.
Il est possible, pour les patients ayant un RA svre et devant
bnficier dune chirurgie non cardiaque en urgence, de proposer
soit une dilatation de la valve aortique [30], soit la mise en place
dune valve aortique percutane (TAVI ou transcatheter aortic
valve implantation) [30, 32]. Les deux types dintervention permettent daugmenter la surface de la valve aortique avec un meilleur rsultat pour le TAVI par rapport la dilatation.
Il faut attirer lattention des cliniciens quun nombre croissant
de publications fait tat du fait que le RA svre induit une maladie de von Willebrand acquise, en relation avec la destruction
des multimres de facteur von Willebrand cause des forces de
cisaillement induites par le RA [33]. Le caractre hmorragique
de cette anomalie de lhmostase, mme dans le contexte dune
chirurgie haut risque hmorragique comme la chirurgie cardiaque nest pas retrouv par tous les auteurs [34].
CARDIOMYOPATHIE HYPERTROPHIQUE OBSTRUCTIVE (CMO)
La CMO est une entit nosologique spare mais elle peut poser
lanesthsiste des problmes similaires ceux du RA svre. La
228
ANESTH S IE
Tableau 40-XVI
Physiopathologie des valvulopathies et objectifs hmodynamiques en pri-opratoire, daprs [29].
Valvulopathie
Adaptation
Consquences
de ladaptation
Histoire naturelle
Facteurs hmodynamiques
aggravants
Objectifs pri-opratoires
Rtrcissement aortique
Hypertrophie VG
Diminution de
la compliance VG
Augmentation de la MvO2
Diminution de
la perfusion coronaire
Longtemps
asymptomatique.
Les manifestations
cliniques (syncope)
sont un signe de
gravit
Hypotension artrielle
(risque dischmie
myocardique)
Perte du rythme sinusal
Tachycardie
Maintien la prcharge
ventriculaire gauche,
du rythme sinusal,
de la pression de
perfusion coronaire
Prvenir laugmentation
de la MvO2 (FC et PAM)
Rtrcissement mitral
Augmentation de la
pression dans lOG
En amont : dilatation,
hypertension veineuse
puis artrielle
pulmonaire post
puis prcapillaire);
insuffisance
ventriculaire droite
En aval : fibrose du VG
et diminution de la
compliance
Longtemps peu
symptomatique
volution rapide (en
3ans aprs apparition
des premiers
symptmes)
Perte du rythme
sinusal, tachycardie,
hypovolmie
Facteurs qui aggravent
lHTAP (hypoxmie,
hypercapnie, acidose)
Maintien du rythme
sinusal et de
la prcharge
ventriculaire gauche
Correction rapide des
facteurs capables
daggraver lHTAP
Insuffisance mitrale
Hypertrophie excentrique
du VG
Augmentation de la taille
de lOG
Diminution du gradient
de pression entre VG
et OG
Maintien du VES
Longtemps
asymptomatique
Hypertension artrielle
Facteurs qui aggravent
lHTAP
Diminution de
la postcharge du VG
Prvention et correction
rapide des facteurs
capables daggraver
lHTAP
Insuffisance aortique
Dilatation du VG
Augmentation du volume Longtemps
Augmentation de la
tldiastolique
asymptomatique
compliance du VG
Maintien du VES
Les signes cliniques
Hypertrophies
vers laval par un
apparaissent lorsque
excentrique et
quilibre complexe
la fonction systolique
concentrique (car
entre maintien de la
est altre (FEVG
surcharge mixte en
rserve de prcharge,
<60% au repos) ou
volume et en pression)
hypertrophie du VG et
lorsque la PTDVG est
augmentation de la
excessive
postcharge
Hypertension artrielle,
bradycardie
Diminution de
la postcharge du VG
FC : frquence cardiaque ; FEVG : fraction djection ventriculaire gauche ; HTAP : hypertension artrielle pulmonaire ; MvO2 : consommation myocardique en oxygne ; OG : oreillette gauche ;
PAM : pression artrielle moyenne ; PTDVG : pression tldiastolique ventriculaire gauche ; VES : volume djection systolique ; VG : ventricule gauche.
CMO a comme consquence une gne ljection ventriculaire

gauche qui entrane une hypertrophie ventriculaire et une diminution de la compliance ventriculaire gauche. La CMO rend le
VG sensible lhypovolmie et dpendant du remplissage auriculaire et du rythme sinusal. Dans certaines situations, il existe un
dplacement antrieur de la valve mitrale pendant la systole ventriculaire (systolic anterior motion ou SAM des Anglo-Saxons) qui
peut entraner une insuffisance mitrale et aggraver lobstruction.
Plusieurs facteurs comme lhypovolmie, la tachycardie, les mdicaments inotropes positifs, lanmie, la vasodilatation peuvent
aggraver lobstruction intraventriculaire. La diminution chronique de la compliance ventriculaire a comme consquence des
pressions de remplissage ventriculaires leves qui peuvent faussement orienter le diagnostic vers une diminution de la contractilit,
ladministration de mdicaments inotropes positifs et laggravation de la situation hmodynamique. Le diagnostic est fait par
lchographie qui permet dobjectiver lobstruction intraventriculaire, les anomalies de la cintique de la valve mitrale (SAM)
et lhypovolmie ventuelle. Pour les patients avec une CMO
diagnostique en propratoire, les objectifs pendant lanesthsie
sont similaires ceux des patients ayant un RA. Dans une tude
rtrospective sur des patients ayant une CMO et une chirurgie
non cardiaque, les complications cardiovasculaires graves (dcs,
infarctus du myocarde, troubles du rythme menaant le pronostic

vital) taient rares (1IDM et un 1trouble du rythme grave sur
77patients) [35]. Nanmoins, 43% des patients avaient fait une
complication cardiovasculaire postopratoire (insuffisance cardiaque 16%; ischmie myocardique 12%; troubles du rythme
sans anomalies de la pression artrielle 25%; hypotension artrielle transitoire 14% [35]). Lincidence des complications priopratoires tait plus importante en cas de chirurgie lourde, mais
26% des patients ayant eu une chirurgie mineure avaient prsent
des complications hmodynamiques pri-opratoires. Les caractristiques chographiques et lampleur de lhypertrophie myocardique ntaient pas statistiquement corrles avec lincidence
des complications hmodynamiques [35].
RTRCISSEMENT MITRAL (RM)
Le RM est le rsultat de la diminution de la surface de lorifice

mitral [29]. La surface mitrale normale chez ladulte est de 4-6cm2.
En dessous de 2-2,5 cm2 (RM modr), le flux transmitral est
conserv par une augmentation modre de la pression dans loreillette gauche (OG). Une surface mitrale >1,5cm2 nentrane pas
de symptmes au repos. Lhistoire naturelle du RM est caractrise
par une longue priode asymptomatique qui peut durer 20-40ans.
Aprs lapparition des premiers symptmes, une priode denviron
10ans scoule avant lapparition des symptmes invalidants [29].

Lorsque la surface mitrale est <1cm2 (RM critique), le flux transmitral et le dbit cardiaque au repos sont assurs par un gradient
denviron 20mmHg (ce qui correspond une pression dans loreillette gauche de 25mmHg). Ceci retentit en amont (dilatation de
loreillette gauche, hypertension veineuse pulmonaire, hypertension artrielle pulmonaire dabord post- et ensuite prcapillaire,
distension puis insuffisance ventriculaire droite) et en aval (diminution du remplissage ventriculaire gauche, fibrose, diminution de la
compliance). En cas dhypertension artrielle pulmonaire (HTAP)
svre (PAPS>60mmHg), la survie moyenne est infrieure 3ans
en labsence dune correction chirurgicale du RM [29]. Tous les
facteurs qui aggravent le gradient transmitral peuvent dstabiliser
la cardiopathie en pri-opratoire.
PROLAPSUS VALVULAIRE MITRAL (PVM)
Le PVM est un syndrome dfini par le prolapsus systolique dune

ou des deux valves mitrales dans loreillette gauche avec ou sans
insuffisance mitrale [29]. Il concerne entre 2 et 6% de la population et dans la majorit des cas il nexiste pas dinsuffisance
mitrale. Nanmoins, le PMV est la premire tiologie dinsuffisance mitrale dans les pays dvelopps [29]. Les PVM primitifs
seraient la consquence danomalies du tissu conjonctif en relation avec des anomalies de lembryogense des lignes cellulaires
msodermiques [29]. Des anomalies similaires au PVM sont
retrouves sur les autres valves cardiaques. Une hyperactivit
sympathique value par des concentrations plasmatiques leves
de noradrnaline et dadrnaline a t rapporte chez les patients
ayant un PVM. Les PVM secondaires peuvent tre associs
des cardiopathies ischmique, rhumatismale, hypertrophique,
des dformations thoraciques (pectus excavatum). Les patients
ayant une maladie de von Willebrand ont une incidence accrue
de PVM. En labsence dune insuffisance mitrale, le pronostic des
patients ayant un PVM est bon avec une mortalit annuelle infrieure 1%. Lapparition de linsuffisance mitrale peut saccompagner dune dilatation de lOG et du VG, de lapparition dune
hypertension artrielle pulmonaire.
Le diagnostic de PVM doit tre voqu en prsence dun click
systolique, ventuellement dun souffle dinsuffisance mitrale, de
palpitations, de douleurs thoraciques atypiques et dantcdents
daccidents ischmiques crbraux. Le reste de lexamen clinique
est habituellement normal, lECG de repos et la radiographie du
thorax sont peu contributifs pour le diagnostic positif ou de gravit. Lchographie cardiaque couple au Doppler est lexamen non
invasif de choix pour lvaluation des patients ayant un PVM mais
les critres diagnostiques chographiques restent controverss [29].
Une paisseur des feuillets mitraux suprieure 5mm est un critre
chographique de gravit associ une augmentation de lincidence
des complications cliniques (endocardite, embolie systmique,
mort subite). Lexistence dune insuffisance mitrale, son retentissement sur les cavits gauches et droites ainsi que les atteintes valvulaires associes sont valus par lchographique cardiaque.
Lorsquil existe une insuffisance mitrale, les patients ayant
un PVM doivent tre considrs comme des patients ayant une
valvulopathie.
Les patients ayant un PVM qui ont fait une complication embolique systmique ont souvent un traitement anticoagulant et antiagrgant plaquettaire dont la gestion en priode pri-opratoire
doit tre ralise en fonction du risque thrombotique/de saignement excessif estim (voir Patients ayant une prothse valvulaire).
229
Les patients ayant seulement des critres chographiques de gravit reoivent souvent de laspirine [29]. Lavis du cardiologue lors
de la consultation pranesthsique est souhaitable si le patient est
symptomatique, sil a dj fait des complications (embolie, endocardite) ou sil a un traitement anticoagulant/anti-agrgant plaquettaire. Le cardiologue doit informer le mdecin anesthsiste
sur lvolution de linsuffisance mitrale, de son retentissement sur
les cavits cardiaques. Les indications opratoires (chirurgie rparatrice mitrale) sont poses de plus en plus tt dans lvolution
des PVM.
INSUFFISANCE MITRALE (IM)
Les principales tiologies des IM sont le PVM, les coronaropathies, les cardites rhumatismales, les anomalies du collagne et
depuis quelques annes certains mdicaments anorexignes [29].
Lincomptence valvulaire mitrale est responsable dune fuite systolique. En cas dIM chronique, il existe une hypertrophie myocardique excentrique compensatrice ayant comme rsultat une
dilatation du VG qui permet le maintien du volume djection
systolique (VES). Le rsultat de la fuite mitrale est une augmentation de la pression et de la taille de lOG. Laugmentation des diamtres des cavits gauches diminue le gradient de pression entre
le VG et lOG ainsi que la pression pulmonaire. La dilatation du
VG est responsable dun VES global augment et dun VES vers
laval normal. cette phase de lvolution, la fraction djection
VG (FE VG) est supranormale (>60%). Ceci expliquerait le fait
quau dbut de lvolution de lIM, la majorit des patients sont
asymptomatiques, mme leffort [29]. En labsence de correction de lIM, la dilatation du VG saggrave, le volume tlsystolique augmente, la pression intra-VG galement. Il sensuit une
augmentation des pressions dans lOG et dans la circulation
pulmonaire responsable de la dyspne, initialement leffort, et
la diminution de la FE VG. Les indications de correction chirurgicale de lIM sont poses actuellement avant lapparition de la
dyspne et des autres signes cliniques (Tableau 40-XVII).
Les IM chroniques, surtout a- ou pauci-symptomatiques,
posent relativement peu de problmes hmodynamiques en priopratoire. Les agents anesthsiques diminuent la prcharge et la
postcharge, le diamtre du VG et favorisent ljection dans le sens
antrograde. Il faut viter les pisodes dhypertension artrielle car
ils peuvent augmenter la postcharge du VG, entraner une dilatation du VG et aggraver lIM. Il est important de comprendre que
le diamtre de lanneau mitral et limportance de la fuite mitrale
sont des phnomnes dynamiques. En prsence dune HTAP,
tous les facteurs capables de laggraver (hypercapnie, hypoxmie,
acidose, augmentation excessive des pressions intrathoraciques)
doivent tre corrigs rapidement.
Le suivi cardiologique rgulier de patients ayant une IM (bilans
cliniques et chographiques annuels) [29] permet au mdecin
anesthsiste destimer lvolution de lIM. Lapparition des symptmes et des signes dHTAP lexamen clinique, sur lECG de
repos et la radiographie de thorax sont des signes indiquant une
volution de lIM. Un patient ayant une IM qui est symptomatique doit tre adress au cardiologue pour correction chirurgicale de la valvulopathie. La prsence dune FE VG <60% doit
toujours alerter le mdecin anesthsiste car la diminution mme
modre (FE VG = 50 % par exemple) signe une volution de
lIM et une altration des conditions de charge du VG. Pour les
patients ayant une IM asymptomatique, lchographie permet de
mettre en vidence une dilatation du VG. Pour ces patients, la
230
ANESTH S IE
Tableau 40-XVII
daprs [29].
Principales indications de chirurgie valvulaire,
Pour le rtrcissement mitral, le traitement de premire intention est la

valvulotomie percutane dont les indications sont : 1) la prsence de symtmes
(NYHA II-IV) et dun RM modr (gradient moyen 5-10mmHg, pression
artrielle pulmonaire systolique entre 30-50mmHg, surface mitrale 1-1,5cm2)
svre (gradient moyen >10mmHg, pression artrielle pulmonaire systolique
>50mmHg, surface mitrale <1cm2 ) et une morphologie de la valve propice
ainsi que labsence de thrombus dans loreillette ou dinsuffisance mitrale
modre svre; 2) une valvulotomie est galement indique chez les patients
asymptomatiques avec PAPS de repos >50mmHg ou deffort >60mmHg;
3) une valvulotomie est indique chez les patients ayant des symptmes
svres (NYHA III ou IV) et pour lesquels le risque chirurgical est considr
comme trop lev, mme en prsence dune valve calcifie. Les indications
chirurgicales (rparation ou remplacement valvulaire) sont : la prsence
dune symptomatologie svre (NYHA III-IV) en prsence dun rtrcissement
modr ou svre lorsquune valvulotomie par ballonnet nest pas disponible
ou est contre-indique cause de la prsence dun thrombus atrial malgr un
traitement anticoagulant ou cause de la prsence dune insuffisance mitrale
ou lorsque lanatomie de la valve mitrale nest pas propice une dilatation ; les
patients en classe NYHAI ayant une surface valvulaire >1,5cm2 mais ayant fait
des pisodes dembolie systmique malgr une anticoagulation adquate.
Pour linsuffisance mitrale, les indications chirurgicales (la rparation est
prfre au remplacement valvulaire) sont : 1) les patients symptomatiques
(NYHA grades II-IV) ayant une insuffisance mitrale sevre (volume rgurgitant
>60mL par battement ou fraction rgurgitante >50%) en labsence dune
altration svre de la FEVG (<30%) et/ou DTSVG>55mm; 2) les patients
asymptomatiques ayant une insuffisance mitrale svre altration modre de
la fonction ventriculaire gauche (30% < FEVG < 60% et un DTSVG >40mm),
les patients asymptomatiques ayant une fibrillation atriale et une fonction
VG prserve, les patients asymptomatiques ayant une fonction VG prserve
et une pression artrielle pulmonaire systolique (PAPS >50 au repos et >
60mmHg leffort). Actuellement, les indications sont largies aux patients
ayant des insuffisances mitrales peu symptomatiques lorsquune chirurgie de
rparation est possible. Les indications sont galement largies aux patients
symptomatiques (NYHA III ou IV) ayant une insuffisance mitrale svre et une
altration svre de la fonction systolique ventriculaire gauche (FEVG < 30%).
Pour le rtrcissement aortique, les indications chirurgicales concernent:
1) les patients symptomatiques quelle que soit la gravit du rtrcissement;
2) les asymptomatiques ayant un rtrcissement svre (surface de lorifice
aortique est < 0,6cm2/m2 de surface corporelle ou 1cm2 ; gradient moyen
>40mmHg ; vlocit du jet > 4m/s) ; 3) les patients asymptomatiques ayant
une altration de la fonction systolique du ventricule gauche, une rponse
anormale leffort (hypotension artrielle), une hypertrophie ventriculaire
gauche (> 15mm). Le remplacement valvulaire aortique est galement
recommand chez les patients ayant un rtrcissement aortique svre
et devant bnficier dune chirurgie de revascularisation myocardique ou
dune autre chirurgie valvulaire. Pour les patients dont le risque opratoire
du remplacement valvulaire aortique est considr comme trop important
(mortalit prdite par lEuroSCORE >20%), la mise en place dune valve
aortique percutane (transcatheter aortic valve implantation) est une option
thrapeutique envisager. Enfin, une dilatation de la valve aortique, chez les
patients hmodynamiquement instables ou en cas de chirurgie non cardiaque
urgente, peut tre envisage.
Pour linsuffisance aortique isole, les indications chirurgicales concernent les
patients symptomatiques avec insuffisance considre comme svre (volume
de rgurgitation >60mL par battement ou fraction de rgurgitation >50%)
quelle que soit leur fonction systolique VG (prserve soit FEVG au repos
>50% ou altre soit FEVG au repos <50%) ; les patients asymptomatique
avec FEVG au repos <50% ; les patients asymptomatiques avec FEVG
>50% mais ayant un DTDVG >75mm ou un DTSVG >55mm; les patients
asymptomatiques ayant une FEVG normale au repos, un DTDVG >70mm ou
un DTSVG >50mm mais avec une rponse anormale lexercice physique ou
en prsence dune dilatation rapide du VG.
DTDVG : diamtre tldiastolique ventriculaire gauche ; DTSVG : diamtre tlsystolique
ventriculaire gauche ; FEVG : fraction djection ventriculaire gauche ; IA : insuffisance
aortique ; IM : insuffisance mitrale ; NYHA : New York heart association; PAPS: pression
artrielle pulmonaire systolique ; RA : rtrcissement aortique ; RM : rtrcissement mitral.
chirurgie non cardiaque pose relativement peu de problmes et la

discussion avec le cardiologue doit porter sur le stade volutif de
lIM, le traitement mdical et lindication de la correction chirurgicale de lIM par rapport la chirurgie non cardiaque.
La dcision de reporter la chirurgie non cardiaque doit tre
prise patient par patient. Ltiologie de lIM doit tre recherche.
Chez les patients gs, ayant des facteurs de risque dathrome
coronarien, lassociation avec une coronaropathie lorigine de
lIM doit tre suspecte et recherche [29].
INSUFFISANCE AORTIQUE (IA) CHRONIQUE
LIA chronique est le rsultat dune surcharge volmique du VG.

Les mcanismes adaptateurs sont : 1) laugmentation progressive
du volume tldiastolique ventriculaire gauche (VTDVG); 2) de la
compliance du VG ayant pour but de maintenir une PTDVG basse;
3) lhypertrophie excentrique et concentrique [29]. Lhistoire naturelle de lIA chronique est caractrise par une progression lente et
une longue priode pendant laquelle les patients sont asymptomatiques. Le diagnostic, voqu par le souffle diastolique et les signes
cliniques habituels est confirm par lchographie qui permet
dexplorer ltiologie, les critres de gravit (quilibration rapide
entre les pressions diastolique aortique et ventriculaire gauche dont
tmoignent un temps de dclration mitrale <150ms et la fermeture prmature de la valve mitrale). Lchographie value aussi le
retentissement de lIA sur le diamtre du VG, sur les cavits droites
ainsi que lapparition dune dysfonction systolique du VG (caractrise par une FE VG<60% au repos). La survie des patients ayant
une IA diminue lorsque le VG est dilat (DTDVG > 75 mm et
DTSVG>55mm) et lorsquil existe une dysfonction systolique
(FE VG < 45 %). Tous ces signes chographiques surviennent
avant les signes cliniques et lindication de correction chirurgicale
de la valvulopathie est pose sur les critres chographiques [29]. Le
risque de complications pri-opratoires (chirurgie non cardiaque)
des patients ayant une IA pour laquelle il nexiste pas dindication
de correction chirurgicale nest pas connu. La survenue dune ischmie myocardique fonctionnelle en relation avec une diminution
de la pression artrielle diastolique redoute est une complication
classique.
valuation propratoire des patients

ayant une valvulopathie
Lvaluation propratoire, fonde sur linterrogatoire, lexamen

clinique et des examens complmentaires (surtout lchocardiographie) doit documenter le diagnostic positif de valvulopathie et estimer sa gravit compte tenu de son histoire naturelle.
partir de lauscultation cardiaque, cest surtout les souffles
diastoliques, holosystoliques ou les souffles associs des signes
cliniques vocateurs de valvulopathie qui doivent attirer lattention en consultation pranesthsique [29]. loppos, les souffles
msosystoliques chez des patients asymptomatiques, non modifis par la manuvre de Valsalva sont moins vocateurs de valvulopathie [29]. Le diagnostic positif de valvulopathie est fait par
lchocardiographie [29] qui permet aussi dtablir le diagnostic
tiologique, le retentissement de la valvulopathie sur les cavits
cardiaques, diamtres ventriculaires gauches, la prsence dune
HTAP avec retentissement sur la fonction ventriculaire droite,
lvaluation de la fonction systolique et diastolique du ventricule gauche. Seront recherchs les modifications rcentes de la
symptomatologie, la prsence de signes cliniques dinsuffisance
cardiaque, (turgescence jugulaire, hpatomgalie, dmes des
membres infrieurs, dme aigu du poumon), les mdicaments

et les doses ncessaires pour stabiliser la symptomatologie. Les
recommandations concernant les doses moyennes et maximales
de diurtiques, dinhibiteurs de lenzyme de conversion, de drivs
nitrs et de digitaliques ont t publies [29]. Lanalyse des doses
de mdicaments et de la symptomatologie permet dapprcier sil
est possible doptimiser la fonction cardiaque par un traitement
mdical. Il est important de documenter le retentissement rnal
et mtabolique (baisse de la clairance de la cratinine, hyponatrmie, hypokalimie, hypomagnsmie) de la valvulopathie et de
son traitement, les pathologies associes (hypertension artrielle,
diabte, bronchopathie chronique obstructive, etc.), la prsence
de troubles du rythme chroniques (fibrillation atriale), ainsi que
lassociation avec une atteinte coronarienne qui peut concerner
jusqu 10% des patients ayant une valvulopathie [29].
La symptomatologie doit tre interprte en fonction de lactivit physique des patients. Lvaluation de lactivit physique peut
faire appel soit la classification de la New York heart association,
soit des critres plus quantitatifs comme le score de Duke (voir
Tableau 40-VII).
la fin de lvaluation propratoire, le mdecin anesthsiste-ranimateur peut classer le patient en une catgorie risque
(Tableau 40-XVIII). Lintervention chirurgicale et lacte anesthsique doivent tre reports si le patient a un souffle cardiaque
organique (voir les critres dcrits plus haut) et na pas bnfici
dun bilan diagnostique du souffle ou lorsque la valvulopathie
dj documente na pas bnfici du suivi adquat (bilan cardiologique datant de plus de 4-12mois selon le type et la gravit de
la valvulopathie) [29]. Cette attitude semble dautant plus licite
quil sagit dun souffle compatible avec le diagnostic de rtrcissement aortique (a fortiori sil est svre et symptomatique) cause
du risque accru dinstabilit hmodynamique pri-opratoire. Si
lintervention est reporte et le patient adress au cardiologue
pour complment de bilan, celui-ci doit rpondre aux questions
concernant lventuel recours une correction chirurgicale de la
valvulopathie ainsi que le traitement mdical optimum.
Il est galement licite de reporter lintervention chirurgicale et
lanesthsie pour les patients pour lesquels le mdecin anesthsiste
suspecte que la valvulopathie a atteint le stade des indications de
correction chirurgicale. Les indications chirurgicales cardiaques
communment admises pour les patients ayant des valvulopathies
sont prsentes dans le Tableau 40-XVII. Nanmoins, les indications chirurgicales actuelles sont complexes et lanesthsiste ne
doit pas hsiter demander lavis des cardiologues avant de reporter la chirurgie non cardiaque. Ainsi, pour linsuffisance aortique
ou mitrale, les indications de correction chirurgicale sont actuellement poses sur lvolution chographique, avant lapparition
des symptmes et avant laltration des fonctions ventriculaires
pouvant poser un problme en pri-opratoire. Dans cette situation, un patient peu- ou asymptomatique peut avoir une insuffisance valvulaire importante, une dilatation modre des cavits
ventriculaires gauches et une indication de correction chirurgicale de la valvulopathie. Ce type de patient possde nanmoins
une rserve fonctionnelle cardiaque qui pourrait lui permettre de
passer le cap dune chirurgie non cardiaque.
En pratique, lors de la consultation danesthsie, il est important, partir de lexamen clinique, de dtecter les patients ayant
une valvulopathie, de reporter lintervention des patients pour
lesquels la valvulopathie est suffisamment svre pour bnficier dune correction chirurgicale, doptimiser le traitement
231
Tableau 40-XVIII Risque de complications cardiovasculaires priopratoires en fonction des valvulopathies et de leur gravit, daprs
[6, 7].
Risque lev (> 5 % de morbidit et mortalit) :
insuffisance cardiaque congestive dcompense ;
valvulopathie svre (rtrcissement aortique de surface < 0,75cm2,
rtrcissement mitral de surface < 1 cm2, insuffisance mitrale et
insuffisance aortique > 3/4), a fortiori en cas de symptomatologie
clinique et/ou dhypertension artrielle pulmonaire.
Risque modr (< 5 % de morbidit et mortalit) :
antcdents de dcompensation cardiaque mais fonction cardiaque
stabilise au moment de lintervention ;
valvulopathies moins svres que celles voques plus haut.
Risque faible :
valvulopathie sans retentissement sur les cavits cardiaques (par
exemple : insuffisance mitrale ou insuffisance aortique de grade I).
des patients qui ont des signes dinsuffisance cardiaque systolique ou diastolique. Lorsque la valvulopathie nest pas suffisamment svre pour ncessiter une correction chirurgicale, la
prise en charge pri-opratoire est fonde sur un raisonnement
physiopathologique.
Prophylaxie de lendocardite bactrienne
Les indications dantibioprophylaxie ont fait lobjet de recommandations rcentes qui ont considrablement restreint les situations o une prophylaxie est ncessaire (Tableau 40-XIX). Les
protocoles dantibioprophylaxie recommands sont prsents
dans le Tableau 40-XX.
Prise en charge des patients ayant une prothse

valvulaire
Ces patients ont un suivi cardiologique rgulier [29]. La prise en

charge pri-opratoire de ces patients est centre sur la prophylaxie de lendocardite [29, 36] (voir Tableaux 40-XIX et 40-XX)
et la gestion du traitement anticoagulant dans la priode priopratoire. Lvaluation propratoire doit permettre destimer
la capacit leffort du patient, de rechercher dventuels signes
dinsuffisance cardiaque ainsi que les ventuelles complications
lies au traitement. Tous les patients ayant une prothse mcanique ont un traitement anticoagulant oral [37]. Les patients
ayant des bioprothses reoivent un traitement anticoagulant
pendant les trois premiers mois qui suivent le remplacement valvulaire et ventuellement par la suite en cas dindications lies
la cardiopathie sous-jacente (dilatation de loreillette, fibrillation
atriale, antcdents dembolies systmiques).
GESTION PRI-OPRATOIRE DU TRAITEMENT ANTICOAGULANT
CHRONIQUE
Lanticoagulation au long cours des patients ayant une prothse

valvulaire est codifie [37]. La gestion de lanticoagulation en
priode pri-opratoire a fait lobjet de recommandations en 2012
[38]. Le traitement par antivitamines K (AVK) ou par anticoagulants oraux directs (AOD) comme le dabigatran, le rivaroxaban
ou lapixaban dans la fibrillation atriale peut tre interrompu
chez les patients ayant un faible risque de complications thromboemboliques pri-opratoire. Chez les patients ayant un risque
thromboembolique lev, le traitement par AVK ou AOD doit
232
ANESTH S IE
Tableau 40-XIX Recommandations concernant la prophylaxie de

lendocardite infectieuse, daprs [36].
Lantibioprophylaxie ne doit tre envisage que pour ces
cardiopathies et seulement pour la chirurgie dentaire avec
intervention gingivale ou de la rgion pri-apicale de la dent
ou pour perforation de la muqueuse orale. La prophylaxie
de lendocardite infectieuse nest pas recommande pour:
bronchoscopie, laryngoscopie, intubation nasale ou trachale ;
gastroscopie, colonoscopie, cystoscopie, chographie transsophagienne ;
chirurgie de la peau et des tissus mous.
Prothses valvulaires
Antcdents dendocardite infectieuse
Cardiopathies congnitales
cardiopathies congnitales non rpares y compris celles ayant fait
lobjet dun traitement par shunts palliatifs
cardiopathies congnitales ayant fait lobjet dun traitement curatif
avec matriel/dispositif prothtique quil ait t mis en place
chirurgicalement ou de manire percutane, surtout dans les 6 mois
aprs la mise en place
cardiopathies congnitales qui ont fait lobjet dun traitement curatif
mais avec persistance dune anomalie au site de rparation ou ct de
matriel prothtique (qui inhibe lendothlialisation)
Transplants cardiaques qui dveloppent une valvulopathie
tre relay. Le relais est dfini par la prescription danticoagulants

en intraveineux ou en sous-cutan, pour une priode de plusieurs
jours pendant la priode dinterruption dAVK pendant laquelle
la valeur dINR (international normalised ratio) nest pas dans les
limites thrapeutiques. Le relais est ralis par un traitement anticoagulant en intraveineux (hparine non fractionne avec comme
objectif thrapeutique un temps de cphaline avec activateur
de 1,5-2 fois les valeurs tmoin ou une concentration de 0,3UI
anti-Xa) ou en sous-cutan par hparine de bas poids molculaire
(par exemple noxaparine 1mg .kg1 deux fois par jour). Larrt
de lhparine non fractionne doit tre fait 4-6 heures avant
Tableau 40-XXI
Tableau 40-XX Propositions dutilisation des antibiotiques pour la

prophylaxie de lendocardite infectieuse.
Situation
Antibiotique
Adulte
Pas dallergie aux

btalactamines
Amoxicilline ou
ampicilline
2g per os ou IV
Allergie aux
btalactamines
Clindamycine
600mg per os
ou IV
Enfant
50 mg . kg1
per os ou IV
20mg . kg1
per os ou IV
IV : intraveineux.
lintervention; la dernire injection dhparine de bas poids molculaire doit tre ralise 24heures avant lintervention. La reprise
du traitement par hparine de bas poids molculaire et risque de
saignement en relation avec lintervention, la premire injection
dhparine de bas poids molculaire doit tre faite 48-72heures
aprs lintervention. Le relais peut tre fait avec des doses plus
faibles (par exemple noxaparine 40mg/jour habituellement utilis pour la prvention de la maladie thromboembolique postopratoire) ou intermdiaires (40mg deux fois par jour).
Chez les patients ayant un risque thromboembolique intermdiaire, la dcision de pratiquer un relais par un anticoagulant
administr en intraveineux ou en sous-cutan est fonde sur
lanalyse des facteurs individuels et des facteurs lis la chirurgie,
ainsi que sur les prfrences du patient. Chez les patients recevant
un traitement par AVK et devant bnficier de soins dentaires
mineurs, il est recommand de continuer les AVK et dutiliser un
mdicament pro-hmostatique par voie orale ou dinterrompre les
AVK 2-3jours avant la procdure. Chez les patients recevant un
traitement par AVK et devant bnficier dune chirurgie superficielle, il est recommand de continuer les AVK et doptimiser
lhmostase chirurgicale. Chez les patients recevant un traitement
par AVK et devant bnficier dune chirurgie pour cataracte, il est
recommand de continuer les AVK.
Estimation du risque thromboembolique pri-opratoire, daprs [38].
Niveau de risque
Antcdents de maladie
thromboembolique
Prothse valvulaire mcanique
Fibrillation atriale
lev (risque de complications

en labsence de traitement
anticoagulant >10%/an)
Tout type de prothse mitrale

Tout type de prothse aortique bille
ou disque
AVC ou AIT datant de moins de 6 mois
Valeur du score CHADS2 5-6

AVC ou AIT datant de moins de 3 mois
Pathologie valvulaire rhumatismale
vnement thromboembolique datant

de moins de 3 mois
Thrombophilie svre (dficit en
protine C, S ou en antithrombine;
anticorps antiphospholipides,
anomalies multiples)
Modr (risque de complications

anticoagulant 5-10%/an)
Prothse aortique ailettes et au

moins un des facteurs de risque
suivant : fibrillation atriale,
antcdents dAVC ou dAIT,
hypertension artrielle, diabte,
insuffisance cardiaque chronique,
ge > 75ans
Valeur du score CHADS2 3-4

entre 3 et 12 mois
Thrombophilie non svre (mutation
htrozygote facteur V Leiden
ou mutation du gne de la
prothrombine)
vnements thromboemboliques
rptition
Cancer actif (traitement dans les
6derniers mois ou traitement
palliatif)
Faible (risque de complications

anticoagulant < 5%/an)
Prothse aortique ailettes sans

fibrillation atriale et sans autres
facteurs de risque dAVC
Valeur du score CHADS2 0-2 (en

labsence dantcdents dAVC ou
dAIT)

de plus de 12 mois et pas dautres
facteurs de risque
AIT : accident ischmique transitoire ; AVC : accident vasculaire crbral ; le score CHADS2= insuffisance cardiaque chronique (1 point), hypertension artrielle (1 point), ge >75ans (1 point),
diabte (1 point), AVC ou AIT (2 points).
Une proposition de gestion pri-opratoire du traitement anticoagulant [39] a t expose prcdemment. Cette proposition
tient compte des risques thromboembolique (Tableau 40-XXI)
et hmorragique (Tableau 40-XXII) pri-opratoires [38]. Trois
principes doivent la guider: 1) diminuer, autant que possible, les
priodes danticoagulation suboptimale ou disocoagulation. Une
fentre de 12-24heures disocoagulation expose probablement le
patient un risque thrombotique relativement faible mais proportionnellement plus important pour une prothse mcanique
en position mitrale quaortique ; 2) analyser patient par patient
le rapport bnfice/risque du saignement excessif pri-opratoire
(anticoagulation excessive pour le type de chirurgie et la technique
danesthsie utiliss) et le rapport du risque de thrombose valvulaire
(anticoagulation suboptimale volontaire); 3) informer le patient
des risques respectifs et lui expliquer la dmarche du rapport bnfice/risque. Les prfrences des patients sont actuellement prises en
compte [40]; ils choisissent en gnral daccepter un risque hmorragique accru pour viter un risque thromboembolique.

des patients ayant des troubles
du rythme ou de la conduction
lincidence des troubles du rythme
et de la conduction en pri-opratoire
Les troubles du rythme (TDR) sont relativement frquents en

pri-opratoire en fonction du type de TDR considr et du type
de chirurgie. Lincidence rapporte (tous types confondus) tait
de 70% dans une srie de 17201 patients (dont 90% taient ASA
1 ou 2) randomiss pour recevoir en entretien dune anesthsie
gnrale avec lenflurane, lhalothane, lisoflurane ou le fentanyl.
Les TDR supraventriculaires (TDRSV) sont les plus frquents.
Dans ltude de Polanczyk et al. [41], les TDRSV pri-opratoires
concernaient 7,6% dune srie de 4181 patients. Une incidence
de 2% tait rapporte en peropratoire strict. Une incidence plus
leve des TDRSV (surtout de la fibrillation atriale), pouvant
aller jusqu 30% a t rapporte en chirurgie thoracique pulmonaire et sophagienne [42].
Tableau 40-XXII Estimation du risque hmorragique pri-opratoire,
daprs [38]. Les chirurgies suivantes sont considres comme
tant haut risque hmorragique en cas de prise danticoagulants
et/ou dagents antiplaquettaires.
Chirurgie urologique
rsection transurtrale de prostate
rsection de vessie
ablation tumorale
nphrectomie
biopsie rnale
Implantation de stimulateur cardiaque ou de dfibrillateur avec un risque
dhmatome dans la poche du dispositif
Rsection de polypes coliques, surtout sessiles, de grande taille (1-2 cm) avec
risque de saignement li la chute descarre
Chirurgie des organes richement vasculariss (rein, foie, rate)
Rsection intestinale avec risque de saignement au niveau des anastomoses
Chirurgie majeure avec dgts tissulaires tendus (chirurgie oncologique,
prothses de hanche et de genou, chirurgie plastique reconstructrice)
Chirurgie cardiaque, intracrnienne, mdullaire/rachidienne
233
Les patients ayant des antcdents de TDR ou de la conduction ont un risque accru de complications cardiovasculaires priopratoires, souvent parce que le TDR ou de la conduction est le
reflet dune cardiopathie sous-jacente. Les principes pour la prise
en charge de ces patients sont les suivants: valuation propratoire, choix dune stratgie anesthsique qui interfre le moins
avec la pathologie sous-jacente et surveillance postopratoire
adapte la cardiopathie. La physiopathologie, le diagnostic et le
traitement des TDR et de la conduction survenus en pri-opratoire ont fait lobjet dune revue exhaustive [43].
lments de physiopathologie des troubles

du rythme et de la conduction
Les brady-arythmies, surtout lorsquelles saccompagnent de la

perte du rythme sinusal diminuent le dbit cardiaque et les performances cardiovasculaires avec des consquences dautant plus
graves que les patients ont dj une cardiopathie sous-jacente. Les
tachy-arythmies diminuent le remplissage ventriculaire, le dbit
cardiaque et peuvent entraner une hypotension artrielle. La diminution du DSC par rduction de la dure de la diastole et laugmentation de la MvO2 peuvent entraner une ischmie myocardique.
Les arythmies sont le rsultat soit dune activit automatique
anormale (en relation avec des pace-makers en dehors du nud
sinusal non inhibs par la dpolarisation physiologique ou en relation avec des postdpolarisations ou PD), soit dune anomalie de
la conduction. Les anomalies en relation avec la prsence de pacemakers ectopiques sont connues. Les PD sont des oscillations du
potentiel de membrane qui suivent le potentiel daction ou qui surviennent lors des dpolarisations partielles des cellules cardiaques.
Lorsque lamplitude dune PD est suffisante, elle peut initier un
potentiel daction et tre lorigine dune activit dclenche. Il
existe deux types de PD: les PD prcoces (phase2 ou 3 du potentiel
daction) et les PD tardives (aprs la repolarisation complte). Les
PD prcoces peuvent tre lorigine des tachycardies ventriculaires
et des torsades de pointe. Les PD tardives peuvent tre conscutives
au traitement par la digoxine, les catcholamines ou la prsence
dune ischmie myocardique. Les PD sont en relation avec une surcharge calcique cellulaire. Le traitement de cette surcharge calcique
est dabord tiologique (traitement dune ischmie, dune stimulation sympathique excessive endogne ou pharmacologique) et, en
mme temps, pharmacologique par lutilisation des antagonistes
des canaux calciques ou de lidocane qui aura comme effet une inhibition des courants sodiques rapides.
Les anomalies de la conduction sont lorigine des circuits de
rentre. Ces circuits peuvent se produire lorsquil existe la fois
une conduction ralentie et un bloc unidirectionnel. En gnral,
ces deux phnomnes sont le rsultat dune diminution du potentiel transmembranaires (ischmie myocardique par exemple).
Prise en charge des patients ayant

un stimulateur cardiaque (SC) ou un
dfibrillateur automatique implantable (DAI)
Lvaluation propratoire [44] a pour buts: 1) de documenter la

prsence dun SC ou dun DAI; 2) didentifier le type de dispositif; 3) de diagnostiquer le fait que le patient est dpendant ou non
de la fonction stimulation antibradycardique ; 4) de connatre
les fonctions actives du dispositif ; 5) de connatre la date du
dernier contrle du dispositif ralis par la cardiologue ; 6) de
connatre les raisons pour lesquelles le dispositif a t implantet
234
ANESTH S IE
les traitements mdicamenteux associs; 7) de connatre le type

de chirurgie/intervention et le risque dinterfrences lectromagntiques (IEM) et danticiper les problmes lis aux IEM (mise
en place de la plaque, type de bistouri utiliser, modification de
la programmation du dispositif avant lintervention). La prise
en charge pr-, peret postinterventionnelle, ainsi que la gestion
des principales complications sont prsentes dans le Tableau
40-XXIII.
PRCAUTIONS PRENDRE EN PEROPRATOIRE
La prsence dun SC ou dun DAI (appels aussi dispositifs dentranement lectrosystolique ou EES), ne justifie pas ladministration
dune prophylaxie de lendocardite, sauf lorsque la cardiopathie
sous-jacente du patient lexige. Le monitorage hmodynamique
invasif est dict par la cardiopathie sous-jacente et le type dintervention. La mise en place dun cathter de Swan-Ganz doit tre vite dans les quatre semaines qui suivent limplantation du dispositif
cause du risque de dplacement des lectrodes endocavitaires.
Il est important de configurer le moniteur ECG pour lui permettre de dtecter les spikes (pointes) de stimulation du dispositif
dEES, de vrifier que le spike dpolarise effectivement le myocarde
et est suivi dune activit lectrique et mcanique myocardique.
Ceci peut tre ralis en monitorant lECG, la pression artrielle
de manire invasive (indication spcifique lie la cardiopathie),
par la courbe de photoplthysmographie dun oxymtre de pouls
ou par la palpation du pouls.
Le monitorage du segment ST de lECG pour le diagnostic
dischmie myocardique est impossible en cas dEES ventriculaire. Dans cette situation, lorsque lischmie myocardique doit
tre monitore en peropratoire, lutilisation de lETO peut tre
envisage avec les problmes de sensibilit, de spcificit et dinterprtation en temps rel inhrents cette technique.
Les mdicaments anesthsiques ne modifient pas le seuil dactivation myocardique. Le seuil peut tre augment par lischmie myocardique, les troubles de lquilibre acido-basique, les anomalies de
lquilibre lectrolytique, ou des concentrations trop importantes
de mdicaments anti-arythmiques. Dans toutes ces situations, il est
possible dobserver un dysfonctionnement du dispositif (il dlivre
le courant lectrique mais ne dpolarise pas le myocarde).
Prise en charge des patients ayant des DAI
Les DAI permettent de dlivrer une nergie suffisante pour traiter

une tachycardie (TV) ou une fibrillation ventriculaire (FV). Un
DAI analyse les intervalles R-R de lECG et les reconnat comme
trop courts ou trop longs [44]. Lorsque plusieurs intervalles R-R
conscutifs sont trop courts, le DAI initie une procdure antitachycardie. Cette procdure peut tre un EES ou un choc. Les
DAI sont galement conus pour lEES en cas de bradycardie. Les
principales indications de DAI, en France, sont prsentes dans le
Tableau 40-XXIV [45].
Les prcautions prendre en propratoire concernant lvaluation des patients sont prsentes dans le Tableau 40-XXIII.

des patients ayant une insuffisance
cardiaque
Linsuffisance cardiaque est une situation physiopathologique
lors de laquelle le cur nest pas capable de pomper un dbit
sanguin adapt aux besoins de lorganisme ou le fait seulement

en prsence de pressions de remplissage leves [46]. En phase
terminale, quelle que soit son tiologie, linsuffisance cardiaque
est souvent due une dfaillance myocardique [46]. Il existe des
situations (le rtrcissement mitral, la pricardite constrictive)
o linsuffisance cardiaque nest pas due une dfaillance myocardique. Environ 30% des patients ayant une insuffisance cardiaque chronique ont une dfaillance diastolique dfinie comme
une surcharge veineuse pulmonaire (ou systmique) en prsence
dune fonction systolique presque normale [46]. Le terme actuel
de ce tableau clinique est linsuffisance cardiaque fonction systolique prserve. Environ 30% des patients insuffisants cardiaques
ont une dfaillance mixte systolique et diastolique et les autres
40% une dfaillance systolique isole [46].
Malgr des progrs considrables dans la prise en charge des
patients insuffisants cardiaques, la mortalit un an est comprise
entre 11-13% chez des patients inclus dans des tudes cliniques
randomises [47]. Dans la population relle, une tude cossaise
publie en 2000 a montr que pour des patients admis lhpital
avec un diagnostic dinsuffisance cardiaque, la mortalit un an
tait de 45% et la survie mdiane tait de seulement 1,4 ans [47].
De surcrot, lge influence de manire notable les effets dltres
de linsuffisance cardiaque sur la survie, en partie en relation avec
lutilisation suboptimale de thrapeutiques prouves comme tant
efficaces [47]. Ces observations expliquent pourquoi, linsuffisance cardiaque, indpendamment de son tiologie, est un facteur
de risque majeur de complications pri-opratoires en chirurgie
non cardiaque. Le vieillissement de la population laisse prsager
une augmentation du nombre de patients ayant une insuffisance
cardiaque [48] et devant bnficier dune intervention chirurgicale et dune anesthsie. Les travaux rcents dmontrent que la
prsence dune insuffisance cardiaque en propratoire est la principale cause de complications cardiovasculaires pri-opratoire
[18, 19]. Il a t suggr que lvaluation propratoire devrait
surtout se concentrer sur linsuffisance cardiaque plutt que sur
la prsence dune coronaropathie [49].
Physiopathologie de linsuffisance cardiaque
En prsence dune dfaillance myocardique ou dune modification des conditions de charge, le cur dispose de plusieurs mcanismes dadaptation pour amliorer la performance myocardique
comme laugmentation de la prcharge (loi de Frank-Starling),
lhypertrophie myocardique ventuellement accompagne de la
dilatation des cavits cardiaques et de lactivation de plusieurs
systme neuro-hormonaux dont le principal but est de maintenir la pression de perfusion systmique (systmes sympathoadrnergique, rnine-angiotensine, et vasopressine). La majorit
des symptmes de linsuffisance cardiaque est en relation avec la
rtention sode destine maintenir la prcharge (dyspne) et
avec la vasoconstriction priphrique musculaire (fatigabilit).
Les traitements de linsuffisance cardiaque chronique (inhibiteurs
de lenzyme de conversion, diurtiques, vasodilatateurs, btabloquants, anti-aldostrone) sont surtout destins attnuer lactivation excessive des systmes neuro-hormonaux qui est bnfique
court terme mais dltre au long cours. la phase terminale de
linsuffisance cardiaque, tous les systmes adaptatifs sont dpasss
et le systme cardiocirculatoire ne dispose daucune rserve fonctionnelle dabord leffort et ensuite au repos [46]. Le contexte
pri-opratoire, cause de laugmentation de la consommation en
oxygne de lorganisme peut tre compar une preuve deffort.
235
Tableau 40-XXIII Principes de prise en charge des patients ayant un stimulateur cardiaque ou un dfibillateur implantable, daprs [44].
valuation printerventionnelle et prparation de lintervention
1) Identifier la prsence dun SC ou dun DAI:
interrogatoire, analyse du dossier mdical, radiographie thoracique, lectrocardiogramme
2) Identifier le type de dispositif :
demander au patient la carte concernant le dispositif, radiographie du thorax, lectrocardiogramme
3) Diagnostiquer le fait que le patient est dpendant de la fonction stimulation antibradycardique
antcdents de brady-arythmie symptomatique, dablation nodale, absence de rythme dchappement aux faibles frquences de stimulation
4) Connatre les fonctions actives du dispositif
le plus souvent par consultation du dossier de cardiologie, discussions avec le cardiologue, interrogations du dispositif
analyse du trac lectrocardiographique
5) Connatre la date du dernier contrle du dispositif ralis par le cardiologue
des recommandations ont t mises quant la priodicit des examens faire par le cardiologue. Linterrogatoire du patient permet destimer le respect de ces
recommandations
6) Connatre les raisons pour lesquelles le dispositif a t implant et les traitements mdicamenteux associs
ceci permet de connatre la cardiopathie sous-jacente et doptimiser la gestion pri-opratoire des traitements mdicamenteux
7) Anticiper le risque dIEM
documente pour bistouri lectrique, ablation par radiofrquence, imagerie par rsonance magntique
possible mais controverse pour radiothrapie, lithotritie
non rapporte pour la thrapie lectroconvulsive
lanticipation dIEM peut entraner les mesures suivantes : reprogrammation du dispositif en mode asynchrone, suspension de certaines fonctions
(asservissement de frquence, antitachyarythmie), utilisation dun bistouri bipolaire, modification de la place de la plaque du bistouri, prsence en salle
dintervention dun aimant et du matriel ncessaire pour raliser un entranement lectrosystolique temporaire et dun dfibrillateur externe
Prise en charge perinterventionnelle

1) Monitorer le fonctionnement du dispositif et du couplage lectromcanique
lectrocardioscopie, palpation du pouls, courbe de photoplthysmographie, pression artrielle invasive si ce type de monitorage est utilis pour dautres
indications pendant lintervention. La mise en place dun aimant sur un stimulateur cardiaque reprogramme, de manire temporaire, le dispositif en mode
asynchrone sans asservissement de la frquence. Nanmoins, leffet de laimant peut tre imprvisible par la programmation initiale et ltat de la batterie. La
frquence en mode asynchrone peut ne pas tre adapte pour un patient donn et leffet de laimant nest pas toujours reproductible. Sur un DAI, la mise en
place de laimant abolit la fonction antitachycardie tout en prservant, le plus souvent, la fonction antibradycardie. Pour la plupart des DAI, il est difficile de
sassurer que leffet de laimant est rel et tous les DAI ne rpondent pas laimant. De surcrot, laimant peut endommager ou modifier de manire durable
la programmation du DAI. Compte tenu de ces rserves, la mise en place de laimant sur un stimulateur cardiaque ou un DAI ne peut pas tre une solution
universelle. Sa prsence en salle est surtout une mesure de gestion en urgence des multiples problmes potentiellement lis ces dispositifs. En situation rgle,
cest linteraction avec le cardiologue qui doit tre la base de la gestion pri-opratoire de ces dispositifs
2) Modifier la gestion du bistouri lectrique: en positionnant la plaque du bistouri lectrique loigner le cheminement du courant du dispositif ; en utilisant un
bistouri bipolaire la place dun dispositif monopolaire ; en vitant lutilisation du bistouri lectrique proximit du dispositif ainsi que lutilisation prolonge et
des niveaux levs dnergie
3) Pour lablation par radiofrquence et la lithotritie, modifier la procdure pour tenir compte de la prsence du dispositif
4) Limagerie par rsonance magntique est en principe contre-indique chez les patients porteurs dun SC ou dun DAI
5) Si une radiothrapie est ncessaire sur le site o est plac le dispositif, il faut le faire dplacer chirurgicalement
Gestion des complications perinterventionnelles

En cas de fibrillation/tachycardie ventriculaire survenant chez un patient ayant un DAI dont les fonctions de dfibrillation ont t inhibes par un aimant ou par
une dprogrammation volontaire avant lintervention, il faut arrter les sources dIEM avant denlever laimant ; analyser le monitorage cardiovasculaire (dont
llectrocardiogramme) pour identifier la reprise de la fonction dfibrillation du DAI lorsque laimant est enlev ; en cas de dprogrammation volontaire, tenter de
reprogrammer en urgence si le programmateur et le personnel ncessaire sont disponibles ; si le DAI sans aimant ou reprogramm ne permet pas la dfibrillation,
utiliser le dfibrillateur externe. Les palettes de dfibrillation doivent tre positionnes le plus loin possible du DAI, de manire perpendiculaire sur le grand axe
du DAI, les plaant dans la mesure du possible en antro-postrieur. Sil est impossible de respecter ces consignes, il faut dfibriller le plus rapidement possible et
prvoir un entranement lecrosystolique par dautres moyens que le DAI
Prise en charge postinterventionnelle

1) Continuer le monitorage de llectrocardiogramme et sassurer que lquipement de dfibrillation externe et dentranement lectrosystoliques sont disponibles en
postopratoire immdiat avant la reprogrammation dfinitive du dispositif
2) Faire vrifier et reprogrammer toutes les fonctions pralablement utilises par le dispositif
DAI : dfibrillateur automatique implantable ; IEM : interfrences lectromagntiques ; SC : stimulateur cardiaque.
236
ANESTH S IE
Tableau 40-XXIV
Principales indications des dfibrillateurs automatiques implantables en France, daprs [45].

Situation clinique
Classe et niveau de preuve
Arrt cardiaque par fibrillation ou tachycardie ventriculaire sans cause aigu ou rversible
I (A)
Patients coronariens sans ou avec symptmes dinsuffisance cardiaque (NYHA II ou III), avec une FEVG < 30 % mesure au moins
30 jours aprs un IDM et 3 mois aprs une revascularisation
I (B)
Tachycardie ventriculaire soutenue, symptomatique sur cardiopathie
I (B)
Tachycardie ventriculaire soutenue spontane, mal tolre, en labsence danomalies cardiaques, pour laquelle un traitement
pharmacologique ou une ablation sont impossibles ou ont chou
I (B)
Syncope de cause inconnue avec tachycardie ventriculaire soutenue ou fibrillation ventriculaire dclenchable, en prsence dune
anomalie cardiaque sous-jacente
I (B)
Patients coronariens avec FEVG entre 31-35% mesure au moins 30 jours aprs un IDM et au moins 3 mois aprs une
revascularisation myocardique avec tachycardie ou fibrillation ventriculaires dclenchables
IIa (B)
Patients ayant une cardiomyopathie dilate primitive NYHA II ou III et avec une FEVG < 30 %
IIa (B)
Maladie gntique haut risque de mort subite par fibrillation ventriculaire sans traitement connu
IIa (B)
Patients en insuffisance cardiaque NYHA III ou IV malgr un traitement optimal avec une FEVG < 35 % et une dure du QRS
>120 ms (indication de DAI avec resynchronisation)
IIa (B)
Patients coronariens avec antcdents dIDM et FEVG entre 31 et 35 %
IIb (C)
Patients ayant une cardiomyopathie dilate primitive en NYHA II ou III et avec une FEVG entre 31 et 35 %
IIb (C)
Tachycardie ventriculaire mal tolre chez un patient en attente de transplantation cardiaque
IIb (C)
Ne sont pas considres comme indications de DAI, les situations cliniques suivantes :
Les syncopes sans cause identifie et sans troubles du rythme dclenchables ; les tachycardies ou fibrillation ventriculaires incessantes malgr le traitement ; les tachycardies ou fibrillations
ventriculaires curables par chirurgie ou ablation ne mettant pas en jeu le pronostic vital ; les tachycardies ou fibrillations ventriculaires aigus ou rversibles (ischmie myocardique,
dyslectrolytmie) ; les arrts cardiocirculatoires secondaires une tachycardie ou fibrillation ventriculaire aves squelles neurologiques graves ou avec une esprance de vie infrieure 1 an ;
la tachycardie ou la fibrillation ventriculaire chez un patient en insuffisance cardiaque terminale et qui nest pas candidat la transplantation cardiaque.
DAI : dfibrillateur automatique implantable; FEVG: fraction djection ventriculaire gauche ; IDM: infarctus du myocarde; NYHA : New York heart association.
Un patient insuffisant cardiaque a des rserves fonctionnelles

diminues ou absentes et ne peut pas rpondre la situation de
stress qui caractrise la priode pri-opratoire.
valuation propratoire des patients

insuffisants cardiaques
VALUATION PROPRATOIRE DES PATIENTS AYANT
DES FACTEURS DE RISQUE DINSUFFISANCE CARDIAQUE
Si les patients ne sont pas connus comme tant insuffisants cardiaques, le diagnostic peut tre voqu en consultation danesthsie sur trois tableaux cliniques isols ou concomitants : 1)
lintolrance leffort ; 2) rtention hydrosode (dmes des
membres infrieurs, distension abdominale); 3) patients asymptomatiques pour les items 1 et 2 avec ou sans signes/
symptmes caractristiques dautres cardiopathies (souffle cardiaque, troubles du rythme) dcouverts lexamen clinque ou
lors dun ECG (onde Q de ncrose, fibrillation atriale), dune
radiographie de thorax qui rvle une pathologie pulmonaire
chronique avec HTAP responsable dun cur pulmonaire
chronique ; dun examen biologique qui rvle un diabte ou
une insuffisance rnale chronique. Lintolrance leffort est
habituellement value par le score NYHA qui va de I (pas de
limitation fonctionnelle) IV (dyspne de repos) mais ce score
a une grande variabilit inter- et intra-observateurs et il existe
des diffrences entre lestimation du score par les patients et les
soignants. Ceci a incit utiliser des tests de tolrance leffort

plus objectifs comme la distance parcourue en six minutes voire
de la mesure de la consommation maximum en oxygne lors dun
test deffort mais ces deux dernires stratgies dvaluation ne
sont pas utilises en routine dans la prise en charge des patients
insuffisants cardiaques et encore moins lors de lvaluation propratoire (stades A et B). En labsence de symptmes (stades
A et B; Tableau 40-XXV), la mise en vidence dune anomalie
cardiaque structurelle (type hypertrophie ventriculaire gauche,
valvulopathie infraclinique) ncessite la pratique dune chocardiographie. Lexamen chocardiographique est par dfinition
exhaustif mais pour le mdecin anesthsiste-ranimateur, il doit
rpondre aux questions suivantes: 1) la prservation/laltration
de la FEVG; 2) la prsence danomalies de la relaxation ventriculaire gauche pouvant diagnostiquer une insuffisance cardiaque
avec fonction systolique prserve ; 3) la prsence dune valvulopathie; 4) la prsence dune HTAP ou dune atteinte ventriculaire droite isole. Ces quatre lments majeurs permettent
de diagnostiquer un patient comme tant insuffisant cardiaque
et destimer le principal mcanisme de linsuffisance cardiaque.
Llectrocardiogramme et la radiographie du thorax contribuent
lvaluation initiale de ces patients avant la pratique dexamens
plus sophistiqus. La mesure de la concentration plasmatique des
peptides natriurtiques comme le BNP (brain natriuretic peptide)
ou de sa partie N-terminale (NT-proBNP) [12] peut aider au diagnostic de linsuffisance cardiaque.
VALUATION PROPRATOIRE DES PATIENTS AYANT

UNE INSUFFISANCE CARDIAQUE DIAGNOSTIQUE
Historiquement, des antcdents dinsuffisance cardiaque saccompagnent dun risque relatif de complications cardiovasculaires graves pri-opratoires (chirurgie non cardiaque) de 2,1
(intervalle de confiance ou IC 95%:1-4,6) [10]. Le risque relatif est de 2,2 (IC 95%: 0,7-6,8) en cas dantcdents ddme
aigu du poumon et de 3 (IC 95%: 1,5-5,9) en cas dinsuffisance
cardiaque dcompense (dme aigu du poumon) [10]. Toutes
manifestations cliniques confondues, les patients ayant une insuffisance cardiaque ont un risque relatif de complications cardiovasculaires graves en pri-opratoire de 3,4 (IC 95%: 2-5,7) [10].
Tableau 40-XXV Stades et prise en charge de linsuffisance
cardiaque, daprs [46].
Stade A
risque dIC (hypertension artrielle, diabte, athrosclrose, obsit,
syndrome mtabolique) mais sans atteinte structurelle cardiaque ou
symptmes dIC
Les objectifs thrapeutiques sont de traiter lhypertension artrielle, les
autres troubles mtaboliques (diabte, syndrome mtabolique), les
facteurs de risque dathrosclrose (dont tabagisme), dencourager
lexercice physique
Les traitements pharmacologiques sont les IEC et les ARA2 dans le cadre
du traitement du diabte ou des pathologies vasculaires
Stade B
Prsence danomalies structurelles cardiaques (antcdents dIDM, prsence
dune hypertrophie ventriculaire gauche, valvulopathies infracliniques)
mais sans signes ou symptmes dIC
Les objectifs thrapeutiques sont ceux du stade A
Les traitements mdicamenteux sont les IEC/ ARA2 et/ou les `-bloquants
chez les patients qui en ont les indications
Les patients au stade B peuvent bnficier dun dfibrillateur automatique
implantable
Stade C
Patients ayant des anomalies structurelles cardiaques avec signes ou
symptmes dIC (dyspne, diminution de la tolrance leffort, fatigabilit)
prsents ou dans les antcdents
Les objectifs thrapeutiques sont ceux des stades A et B avec en plus de la
restriction sode
Les traitements pharmacologiques sont les diurtiques pour corriger la
congestion, les IEC et les `-bloquants. Certains patients peuvent bnficier
dantialdostrones, dARA2, de digitaliques, dhydralazine/drivs
nitrs. Certains patients peuvent bnficier dun stimulateur cardiaque
biventriculaire (resynchronisation interventriculaire) ou dun dfibrillateur
automatique implantable
Stade D
Les patients ont des symptmes dIC au repos malgr un traitement
maximum
Les objectifs thrapeutiques sont ceux des stades A-C auxquels sajoute le
suivi par des quipes spcialises dans la prise en charge des insuffisances
cardiaques terminales
En plus des traitements pharmacologiques du stade C, ces patients peuvent
bnficier dun traitement chroniques par inotropes (dobutamine,
milrinone, lvosimendan), dune transplantation cardiaque, dun dispositif
dassistance cardiaque dfinitif ou en attente dune transplantation, de
chirurgies cardiaques non conventionnelles (dont thrapie cellulaire). Pour
les patients qui ne relvent pas de tels traitements, un accompagnement
palliatif doit tre propos
ARA2 : antagonistes des rcepteurs langiotensine 2 ; IC : insuffisance cardiaque ; IDM :
infarctus du myocarde ; IEC : inhibiteurs de lenzyme de conversion.
237
Lvaluation propratoire des signes et des symptmes des

patients ayant une insuffisance cardiaque doit tre interprte
en tenant compte de son stade et des traitements en cours (voir
Tableau 40-XXV). Elle comporte: 1) la dtection des patients qui
ont une dcompensation de leur insuffisance cardiaque (dme
aigu du poumon par exemple). Cette dmarche est fonde sur linterrogatoire (aggravation de la dyspne deffort, prsence dune
orthopne), lexamen clinique (pression artrielle, frquence cardiaque, signes ddme aigu du poumon, galop, prsence dune
turgescence jugulaire, dune hpatomgalie, ddmes priphriques, de signes de vasoconstriction priphrique) et sur la radiographie de thorax. Les examens biologiques doivent rechercher
une insuffisance rnale fonctionnelle et une hyponatrmie [50].
En dehors dune intervention chirurgicale pour une pathologie qui met en jeu le pronostic vital, il est ncessaire de stabiliser
ces patients en retrouvant la/les cause(s) de dcompensation et
en faisant appel au traitement symptomatique classique (diurtiques, vasodilatateurs) ; 2) pour les autres patients insuffisants
cardiaques, linterrogatoire doit estimer les capacits leffort
du patient partir soit de la classification NYHA soit partir de
lchelle de Duke. Il est important de rechercher les modifications
rcentes de la symptomatologie, lhistoire thrapeutique en fonction de principes actuels de traitement de linsuffisance cardiaque
chronique [46] (voir Tableau 40-XXV).
Lorsque la symptomatologie rcente est compatible avec une
aggravation et lorsque larsenal thrapeutique nest pas complet
ou indique un sous-dosage, il est souhaitable denvoyer le patient
au cardiologue. Il sagit typiquement de patients qui ne reoivent
pas dinhibiteurs de lenzyme de conversion ou des btabloquants
ou dont les doses de diurtiques sont insuffisantes. Les dlais
ncessaires pour observer un effet du traitement optimis ne sont
pas documents mais sont probablement suprieurs plusieurs
semaines. Le cardiologue doit essayer didentifier les patients
insuffisants cardiaques pouvant bnficier dun traitement tiologique de linsuffisance cardiaque (revascularisation myocardique,
correction dune valvulopathie, etc.).
Conduite de lanesthsie
des patients ayant
une cardiopathie
Prmdication et gestion
des traitements chroniques
La prmdication doit dstabiliser le moins possible le traitement
cardiovasculaire chronique. De manire gnrale les mdicaments
ayant des demi-vies courtes sont donns le jour de lintervention. Les mdicaments ayant des demi-vies longues (digitaliques,
amiodarone) peuvent tre arrts la veille de lintervention. Les
inhibiteurs de lenzyme de conversion (IEC) ou les antagonistes
des rcepteurs de langiotensine II (ARA2) sont souvent arrts
la veille de lintervention, a fortiori si une hypovolmie ou un
risque dhypotension artrielle pri-opratoires sont anticips.
La gestion des agents antiplaquettaires (voir Tableaux 40-XIV et
40-XV) et des anticoagulants (voir Tableaux 40-XXI et 40-XXII)
a t aborde prcdemment.
238
ANESTH S IE
Monitorage pri-opratoire
Monitorage de lischmie myocardique
La capacit des diffrents moyens de monitorage dtecter les

consquences de lischmie myocardique dpend de la gravit
de lischmie. Une ischmie myocardique sous-endocardique
non tendue (dfinition anatomique et non ECG) entrane des
troubles de la contractilit segmentaire (dtectables en chocardiographie), qui peuvent ne pas tre dtects par lECG de surface et qui ne sont pas accompagns de troubles de la compliance
ventriculaire gauche (monitorage de la pression artrielle pulmonaire docclusion ou PAPO). Au contraire, une ischmie tendue,
transparitale, sera dtecte la fois par les modifications de la
contractilit segmentaire, les modifications de lECG (modifications du segment ST), par une augmentation de la PAPO (dysfonction diastolique) et une diminution du volume djection
systolique (VES) et de lindex de travail systolique ventriculaire
gauche (ITSVG) (dysfonction systolique) [51]. Le clinicien souhaite dtecter lischmie myocardique une phase prcoce, alors
quelle na pas encore entran de modifications des fonctions
diastolique et systolique. Dans ce cas de figure, lETO serait, au
moins en thorie, le moyen de monitorage capable de dtecter le
plus grand nombre de modifications de la contractilit segmentaires, censes tre les consquences de lischmie myocardique.
Malheureusement, la dtection chographique des modifications
de la contractilit segmentaire en temps rel est difficile et il existe
de nombreux faux positifs cest--dire des modifications de la
contractilit segmentaire qui ne sont pas dues une ischmie.
UTILISATION DE LLECTROCARDIOGRAPHIE POUR
LE MONITORAGE DE LISCHMIE MYOCARDIQUE PRI-OPRATOIRE
Le monitorage le plus rpandu pour le diagnostic de lischmie

myocardique pri-opratoire est lECG. Le diagnostic ECG de
lischmie myocardique est fait partir des modifications (sous- ou
sus-dcalage) du segment ST. Un sous-dcalage (mesur au niveau
du point J + 60ms mais pouvant tre modifi entre 40 80ms
en fonction de la frquence cardiaque) horizontal ou descendant
est fortement vocateur dischmie myocardique. Un sous-dcalage ascendant est galement vocateur dischmie mais peut tre
rencontr en cas de tachycardie. Un sous-dcalage du segment
ST > 0,1 mV est considr comme diagnostique de lischmie
myocardique. Cette valeur est choisie afin dassurer une sensibilit et une spcificit cliniquement acceptables. Des valeurs seuils
plus faibles ont t suggres (0,01mV) mais les consquences sur
la sensibilit et la spcificit dune telle attitude restent dfinir.
Le sus-dcalage du segment ST mesur au pointJ est diagnostique
dischmie myocardique pour des valeurs>0,2mV. Des modifications de lECG comme linversion symtrique des ondes T ou
lapparition dun nouveau bloc de branche gauche peuvent galement suggrer la prsence dune ischmie myocardique.
Il est habituel de parler de dure ou de nombre dpisodes
dischmie myocardique pri-opratoires. Un pisode dischmie
myocardique est caractris par une dure dau moins une minute
identifiable entre deux tracs ECG normaux. Les modifications
du segment ST ne sont pas utilisables pour le diagnostic dischmie myocardique en cas danomalies propratoires de lECG
comme un bloc de branche gauche, la prsence dun entranement
lectrosystolique, une surcharge ECG diastolique, le traitement
chronique par les digitaliques. Des modifications pri-opratoires de lECG en relation avec des problmes extracardiaques
(louverture du thorax, le mode ventilatoire, lhypothermie, lanmie, des anomalies lectrolytiques) peuvent rendre lutilisation
du segment ST pour le diagnostic de lischmie myocardique
dlicate. En prsence danomalies propratoires du segment ST
(hypertrophie ventriculaire gauche, blocs de branche, etc.), il a t
suggr de considrer toute modification du segment ST dont
lamplitude est > 0,1 mV comme tant compatible avec le diagnostic dischmie myocardique.
Plusieurs problmes du diagnostic ECG de lischmie myocardique, dont le positionnement des lectrodes, sont particuliers
la priode pri-opratoire. Le diagnostic topographique de lischmie myocardique fait appel aux 12 drivations habituelles. Dans
la priode pri-opratoire, les moniteurs affichent en gnral
deux drivations. Les deux drivations le plus souvent utilises
(DII et V5) ont une sensibilit de 80% (par rapport lECG 12
drivations) pour dtecter lischmie myocardique. La sensibilit
augmente 98% lorsque trois drivations (DII, V4 et V5 sont utilises). Un problme particulirement difficile concerne la chirurgie thoracique gauche qui empche la mise en place de drivations
prcordiales gauches. Dans cette situation, la sensibilit de lECG
pour le diagnostic de lischmie myocardique est faible.
Le problme est compliqu par le fait que lECG 12 drivations
possde une sensibilit acceptable (90 %) pour le diagnostic de
lischmie myocardique et de linfarctus du myocarde dans le territoire de lartre interventriculaire antrieure mais de seulement
24% dans le territoire de lartre circonflexe et de 54% dans le
territoire de lartre coronaire droite. En pratique, lECG 12 drivation na pas une sensibilit 100% pour le diagnostic de lischmie myocardique et de linfarctus du myocarde. La diminution du
nombre de drivations dans la priode pri-opratoire a obligatoirement comme consquences une diminution de la sensibilit de
lECG pour le diagnostic de lischmie myocardique.
Compte tenu de ce qui a t dit plus haut, chez un patient ayant
des symptmes vocateurs (hypotension artrielle, dyspne, dme
aigu du poumon, insuffisance cardiaque), le diagnostic dischmie myocardique ne doit pas tre limin sur la base dun ECG
considr comme normal. En peropratoire, le diagnostic dischmie myocardique peut tre fait par lETO. En postopratoire, les
dosages rpts des marqueurs biochimiques de souffrance myocardique comme la troponinepermettent de faire le diagnostic de
souffrance myocardique malgr un ECG considr comme normal.
ANALYSE AUTOMATISE DU SEGMENT ST
La plupart des moniteurs actuels utilisent un trac ECG de base sur

lesquels il est possible de modifier la position du point isolectrique
et du point J. Les modifications du segment ST sont analyses et la
moyenne des amplitudes des modifications est calcule sur plusieurs
complexes ECG. Les moyennes sont ractualises rgulirement et
permettent dafficher sur lcran du moniteur un graphique des
tendances des modifications du segment ST en fonction du temps.
Lanalyse automatise du segment ST est plus sensible pour
dtecter une ischmie myocardique que lanalyse ralise par
lanesthsiste sur lcran du moniteur. Lanalyse automatique
fiable des modifications du segment ST est conditionne par une
rponse en frquence correcte du moniteur. En mode monitorage,
afin dliminer les artefacts, la bande de frquence danalyse est
de 0,5-40Hz. Un diagnostic fiable des modifications du segment
ST ncessite une bande danalyse de 0,05-40 (voire 100)Hz. Les
diffrents moniteurs disponibles sur le march ont une sensibilit et une spcificit denviron 70% (comparaison avec analyse a
posteriori des tracs Holter) pour dtecter lischmie myocardique

[52]. Le microvoltage est un des facteurs majeurs expliquant la
faible performance diagnostique des analyseurs automatiques du
segment ST [53]. La sensibilit de lanalyse du segment ST nest
que de 40 % lorsque lETO est utilise pour monitorer lischmie myocardique. Dans le mme contexte, lECG 12 drivations
a galement une sensibilit mdiocre (25% amliore 40% par
la prise en compte des modifications de londeT) lorsquelle est
compare lETO. Deux moniteurs de marques diffrentes qui
analysent les modifications du segment ST donnent des rsultats
similaires mais pas identiques cause des diffrences dans le mode
danalyse, daffichage et le nombre de drivations analyses.
Le message a retenir est que lanalyse des modifications du segment ST sur lcran des moniteurs mais aussi lanalyse automatise du segment ST sous-estime de manire importante lincidence
relle de lischmie myocardique mme lorsque le gold standard
est lECG 12 drivations. Les performances de moniteurs sont
encore moins bonnes lorsquils sont compars lETO utilise
pour le diagnostic de lischmie myocardique. Nanmoins, lETO
fournit probablement un trop grand nombre de faux positifs pour
le monitorage de lischmie myocardique et les comparaisons des
moniteurs ECG avec lETO doivent rester prudentes.
MONITORAGE DE LISCHMIE MYOCARDIQUE
PAR LCHOCARDIOGRAPHIE TRANSSOPHAGIENNE
Lischmie myocardique entrane des modifications de la

contractilit segmentaire dcrites comme hypokinsie modre,
svre, akinsie ou dyskinsie. Elles concernent la fois la diminution de lpaississement parital et labsence de diminution
du diamtre ventriculaire en systole. Lors de lischmie myocardique, les altrations de la contractilit segmentaire peuvent
survenir avant les modifications ECG. Dans plusieurs tudes
ralises en chirurgie cardiaque ou vasculaire, il a t dmontr
que les anomalies de la contractilit segmentaire survenaient
avant ou en labsence de modifications du segment ST et taient
prdictibles de complications ischmiques postopratoires. Les
comparaisons entre lETO, lECG 12 drivations et le Holter
2 drivations pour dtecter lischmie myocardique chez des
patients de chirurgie vasculaire ont montr que le Holter tait
capable de dtecter deux fois plus dpisodes dischmie que les
autres mthodes. La faible performance de lETO dans cette
tude a t mise sur le compte du caractre intermittent du
monitorage ETO et sur la faible prvalence de la maladie coronarienne chez les patients tudis. La prsence danomalies de
la contractilit segmentaire nest pas spcifique de lischmie
myocardique car elle peut tre rencontre en cas dhypovolmie,
daugmentation de la postcharge, de myocardiopathies [53]. En
chirurgie non cardiaque, lapport diagnostique de lETO pour le
monitorage de lischmie myocardique en prsence du monitorage ECG est faible.
Choix du monitorage de lischmie myocardique

pour un patient donn
Tous les patients ayant une cardiopathie ischmique doivent

bnficier dun monitorage automatique du segment ST de
lECG sur deux drivations qui doivent tre choisies en fonction
des territoires myocardiques risque et du type de chirurgie. La
possibilit dobtenir un trac imprim de plusieurs drivations
serait un avantage. Les autres types de monitorages (cathters de
Swan-Ganz par exemple) nont pas une sensibilit suffisante pour
239
le diagnostic de lischmie myocardique. Lutilisation de lETO

reste limite un faible nombre de patients cause du cot du
matriel, de la ncessit de disposer des mdecins expriments
capables de lutiliser et de la difficult danalyse en temps rel.
Lalgorithme propos est le suivant : lorsque le patient a une
coronaropathie mdicalement contrle et en labsence danomalies de lECG de repos rendant lECG peu informatif pour le
monitorage de lischmie myocardique, une fonction systolique
ventriculaire gauche correcte (FE VG > 40%), lECG peut suffire au monitorage de lischmie peropratoire. Lorsque le patient
a une coronaropathie svre, un ECG de repos anormal (blocs
de branches, etc.) ou surtout lorsque les fonctions systolique et
diastolique sont altres (plusieurs infarctus du myocarde dans
les antcdents et/ou des pisodes dOAP ischmique), il est probable que lapparition dune ischmie myocardique, mme dans
un territoire restreint peut avoir des consquences majeures sur
la fonction ventriculaire gauche. Dans cette situation, un moyen
de monitorage sensible (ETO) de lischmie myocardique semble
prfrable avec les rserves faites plus haut.
Monitorage de la pression artrielle

par cathtrisme artriel
Pour les patients ayant une cardiopathie, il est recommand une

utilisation large du cathtrisme artriel mme lorsque lacte
chirurgical ne le justifie pas lui seul. Pour la chirurgie non cardiaque, le cathtrisme artriel est indispensable pour la neurochirurgie intracrnienne, la chirurgie du phochromocytome. Il est
recommand pour la chirurgie vasculaire majeure, la chirurgie
risque hmorragique quel que soit son type (orthopdique, digestive, carcinologique, etc.). Les moniteurs qui analysent la forme
de la courbe de pression artrielle partir dun cathter artriel
permettent le calcul battement par battement du dbit cardiaque
mais avec une performance diagnostique qui peut tre altre par
les modifications de la compliance artrielle ou la prescription de
vasoconstricteurs [54]. Les moniteurs qui permettent une calibration par une courbe de thermodilution ont une meilleure performance diagnostique que ceux sans calibration [55, 56].
Monitorage pri-opratoire invasif du dbit

et des performances cardiaques chez les patients
ayant une cardiopathie
Les principes du monitorage du dbit cardiaque ont t prsents

dans le chapitre xx.
Les indications pour lutilisation dun monitorage invasif du
dbit cardiaque (cathter de Swan-Ganz ou cathter de thermodilution transpulmonaire) en chirurgie non cardiaque prennent
en compte les facteurs lis aux patient (existence de pathologies
cardiovasculaires, respiratoires, rnales, endocrinienne, infectieuses ou autres qui amputent les rserves fonctionnelles), le
type de chirurgie (risque de modifications hmodynamiques
et de lsions secondaires crbrales, cardiaques, rnales) ainsi
que le contexte local de soins. La dcision dutilisation de ce
type de monitorage doit tre prise patient par patient. Pour
les patients ayant une cardiopathie, le monitorage invasif du
dbit cardiaque pourrait tre indiqu en cas daltration de la
fonction systolique du VG (FE VG < 40 %), dIDM rcent,
de cardiopathie ischmique svre, de valvulopathie, dHTAP,
danticipation de modifications importantes de la volmie ou
des conditions des charges (clampage aortique), lors des tats de
240
ANESTH S IE
choc. Lanticipation dun risque ddme pulmonaire pourrait

tre une indication de monitorage par cathter de thermodilution transpulmonaire pour permettre le calcul de leau extravasculaire pulmonaire.
Monitorage par lchographie

transsophagienne (en dehors de lischmie
myocardique)
LETO couple lutilisation du Doppler continu, puls ou couleur est de plus en plus souvent utilise en chirurgie non cardiaque
pour le diagnostic tiologique de linstabilit hmodynamique
et plus rarement pour le monitorage cardiovasculaire. LETO
permet une estimation rapide, relativement peu invasive et plus
fiable que le cathtrisme cardiaque des variations relatives de
la prcharge ventriculaire gauche, surtout lorsque la compliance
ventriculaire gauche est diminue de manire aigu (ischmie
myocardique) ou chronique (hypertrophie ventriculaire gauche).
Lutilisation de lETO permet aussi une estimation du dbit cardiaque, de la fonction systolique et diastolique du VG, de la fonction valvulaire.
Les principales limites de lETO pour le monitorage cardiovasculaire pri-opratoire sont le cot, la ncessit dun apprentissage long, la quasi-impossibilit dutilisation chez un patient
non anesthsi, la ncessit dune attention soutenue de la part
de lchographiste.
Lincidence des complications (lsions sophagiennes, saignements, paralysie des cordes vocales, arythmies) en relation avec
lutilisation de lETO est de lordre de 3%. Lincidence des complications mineures (traumatisme labial, dysphonie, dysphagie)
est denviron 10%. La mortalit rapporte est de 0,01-0,03%. Les
contre-indications de lETO pri-opratoire sont en rapport avec
la pathologie sophagienne et gastrique.
En pratique, lETO ne peut pas tre recommande comme une
technique de monitorage cardiovasculaire de routine en chirurgie non cardiaque cause de son cot, des difficults danalyse en
temps rel et de ses performances diagnostiques mdiocres. En
revanche, son utilisation doit tre rpandue pour le diagnostic
tiologique de linstabilit hmodynamique en pri-opratoire.
Monitorage non invasif du dbit

et des performances cardiaques
La littrature rcente fait une place importante au monitorage

pri-opratoire non invasif des performances cardiovasculaires qui
permet, en estimant le dbit cardiaque et dautres paramtres calculs, tels que le transport artriel en oxygne (TaO2), doptimiser
les performances cardiovasculaires pri-opratoires. Plusieurs types
de moniteurs fonds soit sur lanalyse de la courbe de pression artrielle, soit partir du signal Doppler aortique mesur en transsophagien et sur les interactions avec le cycle respiratoire pour la
ventilation en pressions positives. Ces moniteurs peuvent calculer
plusieurs indices qui peuvent prdire la rponse lexpansion volmique. Ces indices sont le delta de pression pulse (delta PP) ou le
delta de volume djection systolique (delta VVE) mais ncessitent
une ventilation contrle en pression positive avec des volumes courants suprieurs 8mL . kg1. La leve passive des jambes chez des
patients en ventilation spontane permet galement lestimation de
rponse lexpansion volmique [57]. Plusieurs tudes ont montr
que lutilisation de ce type de monitorage en pri-opratoire tait
associe une optimisation des performances cardiovasculaires et
la diminution de lincidence de certaines complications cardiovasculaires ainsi qu la diminution de la dure de sjour lhpital
[58]. Nanmoins, dautres tudes plus rcentes ont mis en doute ces
rsultats [59], expliquant labsence deffets mesurables de loptimisation cardiovasculaire sur loptimisation des techniques chirurgicales dont celles de rhabilitation acclre [60].
Le choix entre les diffrents types de monitorage cardiovasculaire (Tableau 40-XXVI) doit tre fond sur: 1) la disponibilit
des moniteurs dans un tablissement et la formation du personnel
mdical et paramdical; 2) lanticipation de la dure de linstabilit hmodynamique; si linstabilit hmodynamique est principalement peropratoire, une sonde Doppler transsophagienne,
enleve avant lextubation trachale, est une bonne indication ;
si linstabilit hmodynamique anticipe concerne la priode peret postopratoire, chez un patient extub, lanalyse de la courbe
de pression artrielle reprsente une meilleure indication. Dans
tous les cas de figure, la prsence dune dysfonction ventriculaire
droite, rend lutilisation du deltaPP ou du delta VVE pour la prdiction de la rponse au remplissage inutilisable.
Tableau 40-XXVI Choix du monitorage cardiovasculaire invasif et

du site de surveillance postinterventionnelle en fonction du type de
cardiopathie et de chirurgie.
Risque
chirurgical
Faible
Modr
lev
Risque cardiaque
Faible
Modr
Monitorage non
invasif
Monitorage non
invasif
Surveillance
postopratoire
en salle de
rveil
Surveillance
postopratoire
en salle de
rveil
Monitorage non
invasif
Monitorage non
invasif
Surveillance
postopratoire
en salle de
rveil
Surveillance
postopratoire
en salle de
rveil
Monitorage
invasif de
la pression
artrielle
Surveillance
postopratoire
en salle de
rveil
Monitorage
invasif de
la pression
artrielle
Monitorage par
cathter type
Swan Ganz
Surveillance
postopratoire
en salle de
rveil
USC : unit de surveillance continue.
Elev
Monitorage invasif
de la pression
artrielle ou Doppler
transsophagien
Surveillance
postopratoire en
ranimation/USC
Monitorage invasif
de la pression
transsophagien
Monitorage par
cathter type Swan
Ganz ou un autre
type de monitorage
invasif et calibr du
dbit cardiaque
Surveillance
postopratoire en
ranimation/USC
Monitorage invasif
de la pression
transsophagien
Monitorage par
cathter type Swan
Ganz ou un autre
type de monitorage
invasif et calibr du
dbit cardiaque
Surveillance
postopratoire en
ranimation/USC
Choix de la technique danesthsie

Le choix de la technique anesthsique (locorgionale versus anesthsie gnrale) chez les patients ayant une cardiopathie reste un
sujet controvers, comme pour tous les patients. Lorsquune anesthsie locale ou locorgionale (bloc plexique par exemple) peut
tre utilise, la cardiopathie, par elle-mme, ne reprsente pas une
contre-indication, hormis les situations o la gestion pri-opratoire de lanticoagulation et des agents antiplaquettaires pose un
problme. La controverse concerne le choix entre anesthsie pridurale seule ou en complment dune anesthsie gnrale contre
anesthsie gnrale seule ainsi que le choix des agents anesthsiques pour lanesthsie gnrale.
Place de lanesthsie mdullaire (pridurale

ou rachidienne) chez les patients ayant
une cardiopathie
Les patients ayant une cardiopathie sinscrivent dans la controverse globale concernant les effets de lanesthsie mdullaire
versus lanesthsie gnrale sur la morbidit (ilus postopratoire, diminution des complications respiratoires ou cardiovasculaires) et la mortalit [61]. Une mta-analyse publie en 2009
comparant lanesthsie gnrale et lanesthsie mdullaire dans la
chirurgie prothtique de la hanche ou du genou (tudes publies
entre 1966 et 2008) mettait en vidence un raccourcissement de
la dure dintervention et une diminution du saignement et des
complications thromboemboliques postopratoires mais pas de
diffrence en ce qui concerne les complications graves ni la mortalit [62). Labsence deffet bnfique ou dltre a galement
t mise en vidence lors dune tude rtrospective portant sur
environ 9500 patients qui a compar lanesthsie gnrale et la
rachianesthsie pour chirurgie de la fracture du col du fmur
[63]. Ces observations sont dautant plus surprenantes quil
existe des travaux cliniques qui ont montr que chez des patients
coronariens, lanesthsie pridurale thoracique augmente le diamtre coronaire et amliore la cintique rgionale et globale du
ventricule gauche [64]. Par ailleurs, en chirurgie cardiaque, une
anesthsie pridurale en prsence dune anesthsie gnrale diminue lincidence de lindex composite mortalit et infarctus du
myocarde et de linsuffisance rnale postopratoire [65]. Cette
discordance entre effets bnfiques sur des critres intermdiaires
et absence de bnfice sur la morbidit grave/mortalit a t mise
sur le compte du fait que: 1) les comparaisons ont port la fois
sur lanesthsie pridurale lombaire et thoracique et quil est
document que lanesthsie pridurale lombaire peut avoir des
effets hmodynamiques nfastes en relation avec lhypovolmie et
la redistribution volmique quelle entrane [66]; par comparaison, les effets hmodynamiques de lanesthsie pridurale thoracique seraient plus limits; 2) les tudes ont mlang anesthsie
pridurale et analgsie pridurale; 3) lhypovolmie induite par
lanesthsie pridurale, en mettant en jeu le barorflexe entrane
une activation sympathique et une tachycardie potentiellement
dltres ; 4) il peut exister une mauvaise gestion de la priode
de transition qui suit larrt de lanesthsie/analgsie pridurale;
5)il peut exister un rebond dhypercoagulation larrt de lanesthsie/analgsie pridurale; 6) lanesthsie pridurale peut entraner des anomalies de la rgulation thermique.
Les revues systmatiques et les mta-analyses nont pas mis en
vidence un effet de la technique danesthsie sur la mortalit ni
241
sur la morbidit grave cause des problmes vidents de puissance

statistique, compte tenu de la faible mortalit pri-opratoire
imputable lanesthsie et de lhtrognit des tudes [61]. La
tolrance hmodynamique de lanesthsie mdullaire dpend de
la gravit de la cardiopathie et des traitements associs mais aussi
du niveau du bloc sympathique. Il existe trs peu de publications
qui comparent anesthsie mdullaire ou absence danesthsie
gnrale et anesthsie gnrale chez les patients ayant des cardiopathies svres. Dans une tude publie en 2011 portant sur des
patients ayant des rtrcissements aortiques svres, contre-indiqus la chirurgie cardiaque conventionnelle cause dun risque
de mortalit postopratoire estim comme prohibitif (> 20 %)
[67] qui ont bnfici dune implantation de valve aortique percutane, lanesthsie gnrale, compare une anesthsie locale
supplmente par une sdation base de rmifentanil, tait associe une instabilit hmodynamique dont tmoignait le recours
aux mdicaments cardio- et vaso-actifs (80% dans le groupe anesthsie gnrale versus 20% dans le groupe anesthsie locale avec
sdation; P<0,001) [32].
Avec les rserves faites plus haut sur la mthodologie des tudes,
il nexiste pas de preuves suffisantes ni pour imposer lanesthsie et
lanalgsie mdullaires comme un standard de soins chez les patients
cardiaques, ni pour les rcuser. En pratique, il est rationnel daffirmer que chez les patients ayant une cardiopathie, lanesthsie doit
prserver lquilibre hmodynamique. Cet objectif peut tre atteint
avec diffrentes techniques danesthsie. La technique anesthsique
de choix doit tre celle qui offre le plus grand index thrapeutique
au patient (maximum de bnfices pour le minimum de risque) et
ventuellement le moindre cot. Lindex thrapeutique dune technique est en relation avec la technique elle-mme mais surtout avec
la matrise que lquipe anesthsique en a.
Choix des agents anesthsiques pour

lanesthsie gnrale
Les principes qui doivent guider lanesthsie gnrale pour une

chirurgie non cardiaque risque lev chez les patients ayant une
cardiopathie sont les suivants:1) viter le surdosage anesthsique
cause du risque dinstabilit hmodynamique; 2) viter le sousdosage anesthsique car ceci augmente le risque de mmorisation
explicite postopratoire; 3) prserver les objectifs thrapeutiques
habituels de lanesthsie en ce qui concerne la rapidit du rveil;
en effet, la technique historique danesthsie pour les patients
ayant une cardiopathie (morphiniques haute dose) qui aboutissait avec les morphiniques anciens des dlais de rveil trop longs
a t abandonne. Pour rpondre aux trois objectifs, les patients
ayant une cardiopathie, surtout lorsquils sont insuffisants cardiaques pourraient bnficier du monitorage moderne des effets
des agents anesthsiques par un moniteur qui analyse llectroencphalogramme frontal (par exemple lindex bispectral ou
BIS). Lutilisation du monitorage de la profondeur de lanesthsie permet dviter la fois le surdosage [68, 69] et le sous-dosage
anesthsique qui augmente le risque de mmorisation explicite
chez les patients ayant une cardiopathie svre [70] mais ceci
pourrait ne pas tre le cas chez les patients ayant une cardiopathie moins svre [76]. lextrme, il est possible de dire quavec
le monitorage hmodynamique et de profondeur de lanesthsie,
il nexiste plus de spcificits pour la gestion des mdicaments
anesthsiques. Les cardiopathies sont un des lments pouvant
expliquer la variabilit interindividuelle pour ce qui concerne les
doses/concentrations de mdicaments anesthsiques.
242
ANESTH S IE
CHOIX DES MORPHINIQUES
Il existe un avantage thorique lutilisation du rmifentanil cause

du dlais trs court dquilibration entre la concentration plasmatique et la concentration au site effet (90secondes) et de sa demivie contextuelle courte qui permettent dadapter trs rapidement
les concentrations cibles en fonction du niveau de stimulation
nociceptive pour prvenir/corriger la fois le sous- et le surdosage anesthsique. Une mta-analyse publie en 2012, concernant
lanesthsie en chirurgie cardiaque, a montr un bnfice li lutilisation du rmifentanil sur la diminution de la dure de ventilation
mcanique, de sjour en ranimation et laugmentation postopratoire de troponine [71]. Il nest pas document que ces effets soient
extrapolables aux patients de chirurgie non cardiaque.
CHOIX DES HYPNOTIQUES INTRAVEINEUX
Ltomidate est lhypnotique de choix pour linduction de lanesthsie chez les patients ayant une cardiopathie en raison de sa
bonne tolrance hmodynamique mais ne doit pas tre utilis en
perfusion continue cause du risque dinsuffisance surrnalienne.
La dose dinduction est de 0,3-0,6 mg . kg1. La ktamine reste un
mdicament de choix pour linduction chez les patients en tat de
choc, cause de labsence deffet inotrope ngatif mais il faut peser
les bnfices et les inconvnients de cette molcule chez les patients
ayant une cardiopathie ischmique. Les barbituriques ont un effet
inotrope ngatif qui est dose/concentration-dpendant. Si le propofol est choisi comme agent dinduction, il est recommand de
faire une titration afin dattnuer ses effets hmodynamiques. La
titration consiste dbuter avec une concentration plasmatique
de propofol de 1-1,5 +g . mL1 (AIVOC) et de laugmenter par
paliers de 0,5 +g . mL1. Il est ncessaire dattendre lquilibration
entre les concentrations plasmatique et au site effet avant daugmenter la concentration. La concentration prdite de propofol au
site effet lors de la perte du contact verbal est la premire tape de
la titration. Par la suite, une titration sur la raction hmodynamique et les valeur de BIS lors de la laryngoscopie et de lintubation doit tre ralise [72]. En labsence de lAIVOC, la titration
peut tre faite par une perfusion continue.
Pour lentretien de lanesthsie, lAIVOC pourrait permettre
doptimiser la titration des agents intraveineux chez des patients
ayant une cardiopathie mais une revue systmatique ralise chez
des patients non identifis comme ayant une cardiopathie, na pas
permis de mettre en vidence un bnfice mesurable de lAIVOC
versus titration manuelle pour le propofol [73].
CHOIX DES HYPNOTIQUES ADMINISTRS PAR INHALATION
Lutilisation des halogns comme le svoflurane ou le desflurane pourrait avoir un avantage thorique chez les patients ayant
une cardiopathie car il a t montr quen chirurgie cardiaque,
lutilisation des halogns tait associe une diminution de la
dysfonction myocardique postopratoire et une moindre utilisation de catcholamines [74]. Nanmoins, ces effets nont pas
t retrouvs en chirurgie non cardiaque [75]. Deux tudes ont
montr que lutilisation des alarmes sur les concentrations tlexpiratoires dhalogns correspondant deux fois la concentration de la CAM de rveil (soit 0,3=2=0,6CAM) aboutissait la
mme incidence de mmorisation explicite que celle observe par
lutilisation du BIS [76, 77].
En rsume, il nexiste pas de preuves que le choix de tel ou tel
mdicament anesthsique influence la morbidit et la mortalit
chez les patients ayant une cardiopathie mais certains mdicaments,
surtout par leurs proprits pharmacocintiques, permettent, au

moins dans certaines tudes, de faciliter la gestion de lanesthsie.
Maintien de lhomostasie
Plusieurs actions destines maintenir lhomostasie diminuent
lincidence de lischmie myocardique pri-opratoire. Il sagit du
maintien de la normothermie, de la prvention et de la correction
de lanmie et de lanalgsie.
Prvention de lhypothermie
Lhypothermie pri-opratoire, mme modre (temprature centrale<35C), augmente lincidence des complications ischmiques
[78]. Chez les patients coronariens, le maintien de la normothermie (36,7C en moyenne) diminue de 55% les complications cardiaques par rapport aux patients ayant prsent une hypothermie
modre (35,4C) [79]. Par ailleurs, il a t montr que le maintien
de la normothermie diminuait les besoins transfusionnels [80]. En
pratique, le maintien de la normothermie doit reprsenter un objectif majeur de lanesthsie chez les patients ayant une cardiopathie.
Prvention et correction de lanmie

pri-opratoire chez des patients ayant
une cardiopathie
Lanmie propratoire, y compris pour les anmies modres

(hmatocrite entre 29 et 39%), indpendamment de la transfusion sanguine, est un facteur de risque de complications et de mortalit postopratoires [81]. La transfusion par elle-mme, bien
que corrigeant lanmie, augmente le risque de mortalit [82] et
dinfection nosocomiale. Ces deux observations contradictoires
expliquent pourquoi plusieurs groupes dexperts ont rdig des
recommandations pour la pratique clinique et tous stipulent quil
nexiste pas de valeur seuil universelle qui doit entraner la transfusion homologue [83]. Lorsque le dbit coronaire est limit (stnose
coronaire), mme en normovolmie, lanmie (Hb < 8 g . dL1)
peut entraner une ischmie myocardique [83]. Les donnes
actuelles permettent de dgager quelques recommandations: 1)
la prsence dune ischmie myocardique pri-opratoire oblige le
clinicien sinterroger sur le contenu artriel en oxygne, un des
lments dterminant le TaO2. Des concentrations dhmoglobine infrieures 10g . dL1, mme en normovolmie, peuvent
entraner la prescription dune transfusion homologue; 2) chez
les patients ayant une cardiopathie (surtout coronarienne) et
devant bnficier dune chirurgie risque, il a t montr quune
valeur dhmatocrite <28% augmentait de manire significative
le risque dischmie myocardique postopratoire. Les donnes
actuelles suggrent que la prvention de lanmie et sa correction par lapport en fer [84] est plus efficace que sa correction
pour diminuer lincidence des complications cardiovasculaires
pri-opratoires.
En pratique, il est licite de corriger une anmie (Hb < 9
10g . dL1) chez des patients ayant une coronaropathie dans le
contexte dune chirurgie risque, a fortiori en cas de signes dischmie myocardique. Laugmentation de la concentration dhmoglobine 12g . dL1 na pas permis dobtenir un bnfice sur
la survie. En pri-opratoire, lobjectif chez les patients ayant une
cardiopathie est une concentration dhmoglobine aux alentours
de 10g .dL1 car une concentration trop leve dhmoglobine
pourrait avoir des effets dltres chez les patients coronariens.
Prise en charge postopratoire

des patients ayant une
cardiopathie aprs chirurgie
non cardiaque
Analgsie postopratoire
Lanalgsie est un aspect essentiel de la prise en charge pri-opratoire pour tous les patients et les recommandations faites pour
lanalgsie postopratoire sappliquent sans restrictions aux patients
ayant une cardiopathie. Chez les patients coronariens bnficiant
dune revascularisation coronarienne, un protocole danalgsie
agressif fond sur ladministration de sufentanil saccompagne dune diminution du nombre dpisodes dischmie et de
leur svrit [85]. Il nexiste pas de preuves que lanalgsie pridurale postopratoire, compare lanalgsie contrle par le patient
(morphine) diminue lincidence des complications ischmiques
myocardiques aprs chirurgie aortique [86]. Un problme particulier chez les patients ayant une cardiopathie concerne lutilisation
des anti-inflammatoires non strodiens (AINS) pour lanalgsie
postopratoire. LAHA a publi en 2007 [87] une mise en garde
concernant la prescription de mdicaments analgsiques chez les
patients ayant une cardiopathie. La prescription dAINS (y compris de ceux spcifiques de la cyclo-oxygnase de type 2, les coxibs)
est associe un risque accru de complications (hypertension
artrielle, rtention hydrosode, complications ischmiques myocardiques, complications thromboemboliques) et il a t suggr
dutiliser en priorit le tramadol, lactaminophne et les morphiniques pour traiter la douleur aigu. Il a galement t recommand
dutiliser les AINS aprs analyse du rapport bnfice/risque, de restreindre la dure de prescription et de surveiller lapparition dventuelles complications. Une revue descriptive publie en 2007 [88] a
abord le problme de lutilisation des AINS chez les patients ayant
une cardiopathie et a conclu que: 1) la littrature, malgr de nombreuses limitations, est en faveur dun risque accru cardiovasculaire,
surtout chez les patients risque lev; 2) quil tait prudent danalyser le rapport risque/ bnfice individuellement; 3) que probablement pour le contexte pri-opratoire, en utilisation de courte
dure, le bnfice des AINS est plus important que le risque. En
pratique, les AINS ne doivent pas tre un antalgique de premire
intention chez les patients ayant une cardiopathie dans le contexte
pri-opratoire mais ils ne sont pas contre-indiqus pour une utilisation de courte dure.
Surveillance systmatique
postopratoire des patients ayant
une cardiopathie
Les recommandations Sfar/SFC de 2011 stipulent la surveillance
postopratoire rpte des patients coronariens aprs chirurgie non
cardiaque par lexamen clinique, lECG quotidien, la mesure des
concentrations dhmoglobine et de troponine dans les jours qui
suivent une intervention risque intermdiaire ou leve [5]. Par
extrapolation, le mme type de surveillance peut tre suggr pour
les autres patients ayant une cardiopathie. Il nexiste pas de recommandations concernant le site de surveillance pour ces patients.
243
Les recommandations concernant le dosage rpt de troponine, biomarqueur de dommage myocardique sont fondes sur les
tudes qui ont montr une association statistiquement significative entre la prsence dun dommage myocardique postopratoire
et une augmentation de la morbidit et de la mortalit hospitalire et distance. Dans ce contexte, laugmentation des concentrations plasmatiques de troponine en postopratoire de chirurgie
non cardiaque devient un critre de substitution sur lequel lefficacit des interventions pourrait tre juge. Dans une mta-analyse (14 tudes, 3318 patients, 459 dcs) publie en 2011 [89],
entre 8,4 et 53% des patients qui ont bnfici dune chirurgie
non cardiaque, avaient eu une augmentation des concentrations
de troponine (T ou Ic) en postopratoire ; cette augmentation
tait associe une augmentation statistiquement significative
(OR ajust: 3,4; IC 95%: 2,2-5,2) du risque de mortalit un an
(avec nanmoins une htrognit importante) [89]. Parmi les
patients qui avaient une augmentation de la troponine en postopratoire de chirurgie non cardiaque, seulement 14% avaient eu
une douleur thoracique et seulement 53% des signes/symptmes
cliniques; autrement dit 50% des patients qui ont une augmentation de la troponine aprs chirurgie non cardiaque taient asymptomatiques. Ce rsultat est une justification la ralisation du
dosage rpt de troponine, chez les patients ayant une cardiopathie, a fortiori une coronaropathie, y compris asymptomatiques.
Le dosage rpt de la troponine en postopratoire pourrait
permettre une stratification supplmentaire du risque de complications pri-opratoires par rapport la stratification avec le
score de Lee (propratoire) et du score Apgar chirurgical (stratification postopratoire immdiate). En pratique, cette recommandation pose plusieurs problmes concernant: 1) la slection
des patients qui doivent bnficier dun tel suivi postopratoire;
si tous les patients ayant un score de Lee >2 ou un score Apgar
chirurgical <7 bnficient dun tel suivi, il est probable que ceci
pose des problmes logistiques; 2) les interventions mettre en
uvre aprs mise en vidence dune augmentation de la troponine
en postopratoire.
Il a nanmoins t montr dans le contexte de la chirurgie
prothtique de la hanche que le respect des recommandations
dantibioprophylaxie et de thromboprophylaxie, le dosage rpt
des concentrations plasmatiques de troponine pendant les trois
premiers jours postopratoires, coupl la prvention et la
correction rapide des anomalies de lhomostasie (anmie, hypothermie, infection, hypovolmie, hyperglycmie) ainsi que le traitement de la douleur et la rintroduction rapide en postopratoire
des mdicaments cardiovasculaires dont laspirine, tait associ
une diminution statistiquement significative des complications
cardiovasculaires majeures et de la mortalit [20]. Bien que cette
tude ne soit pas randomise, ses interventions sont fondes soit
sur les recommandations (antibioprophylaxie, thromboprophylaxie), soit sur le maintien de lhomostasie et devraient faire partie de la pratique quotidienne.
En rsum, la prise en charge pri-opratoire des patients ayant
une cardiopathie a volu avec plusieurs tendances rcentes :
1)stratification du risque en pr- et en postopratoire et plus seulement en propratoire; 2) une meilleure comprhension de la
physiopathologie des complications aboutissant moins daccent
sur des interventions uniques (type revascularisation myocardique ou prophylaxie de lischmie myocardique par les btabloquants) et davantage daccent mis sur des approches multimodales
destines prserver lhomostasie et continuer les traitements
244
ANESTH S IE
chroniques. La stratgie anesthsique pure comme le monitorage ou le choix des mdicaments ont peu deffets mesurables
sur lincidence des complications pri-opratoires. Ceci devrait
tre une incitation avoir une approche de mdecine pri-opratoire qui inclue la stratgie anesthsique.
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102. Fleischmann KE, Zegre-Hemsey J, Drew BJ. The new universal
definition of myocardial infarction criteria improve electrocardiographic diagnosis of acute coronary syndrome. J Electrocardiol.
2011;44:69-73.
103. Atkins D, Best D, Briss PA, et al. Grading quality of evidence and
strength of recommendations. BMJ. 2004;328:1490-4.
European Heart Journal Advance Access published August 4, 2014

European Heart Journal
doi:10.1093/eurheartj/ehu282
ESC/ESA GUIDELINES
2014 ESC/ESA Guidelines on non-cardiac surgery:

cardiovascular assessment and management
The Joint Task Force on non-cardiac surgery: cardiovascular
assessment and management of the European Society of Cardiology
(ESC) and the European Society of Anaesthesiology (ESA)
ESC Committee for Practice Guidelines: Jose Luis Zamorano (Chairperson) (Spain), Stephan Achenbach (Germany),
Helmut Baumgartner (Germany), Jeroen J. Bax (Netherlands), Hector Bueno (Spain), Veronica Dean (France),
Christi Deaton (UK), Cetin Erol (Turkey), Robert Fagard (Belgium), Roberto Ferrari (Italy), David Hasdai (Israel),
Arno W. Hoes (Netherlands), Paulus Kirchhof (Germany/UK), Juhani Knuuti (Finland), Philippe Kolh (Belgium),
Patrizio Lancellotti (Belgium), Ales Linhart (Czech Republic), Petros Nihoyannopoulos (UK), Massimo F. Piepoli
(Italy), Piotr Ponikowski (Poland), Per Anton Sirnes (Norway), Juan Luis Tamargo (Spain), Michal Tendera (Poland),
Adam Torbicki (Poland), William Wijns (Belgium), Stephan Windecker (Switzerland).
* Corresponding authors: Steen Dalby Kristensen, Dept. of Cardiology, Aarhus University Hospital Skejby, Brendstrupgardsvej, 8200 Aarhus Denmark. Tel: +45 78452030;
Fax: +45 78452260; Email: steendk@dadlnet.dk.
Juhani Knuuti, Turku University Hospital, Kiinamyllynkatu 48, P.O. Box 52, FI-20521 Turku Finland. Tel: +358 2 313 2842; Fax: +358 2 231 8191; Email: juhani.knuuti@utu.fi
The content of these European Society of Cardiology (ESC) Guidelines has been published for personal and educational use only. No commercial use is authorized. No part of the ESC
Guidelines may be translated or reproduced in any form without written permission from the ESC. Permission can be obtained upon submission of a written request to Oxford University
Press, the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC.
Other ESC entities having participated in the development of this document:
ESC Associations: Acute Cardiovascular Care Association (ACCA); European Association for Cardiovascular Prevention & Rehabilitation (EACPR); European Association of Cardiovascular Imaging (EACVI); European Association of Percutaneous Cardiovascular Interventions (EAPCI); European Heart Rhythm Association (EHRA); Heart Failure Association (HFA).
ESC Councils: Council for Cardiology Practice (CCP); Council on Cardiovascular Primary Care (CCPC).
ESC Working Groups: Cardiovascular Pharmacology and Drug Therapy; Cardiovascular Surgery; Hypertension and the Heart; Nuclear Cardiology and Cardiac Computed Tomography;
Thrombosis; Valvular Heart Disease.
Disclaimer. The ESC Guidelines represent the views of the ESC and were produced after careful consideration of the scientific and medical knowledge and the evidence available at the
time of their dating. The ESC is not responsible in the event of any contradiction, discrepancy and/or ambiguity between the ESC Guidelines and any other official recommendations or
guidelines issued by the relevant public health authorities, in particular in relation to good use of healthcare or therapeutic strategies. Health professionals are encouraged to take the ESC
Guidelines fully into account when exercising their clinical judgment as well as in the determination and the implementation of preventive, diagnostic or therapeutic medical strategies;
however, the ESC Guidelines do not override, in any way whatsoever, the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of the
condition of each patients health and in consultation with that patient and, where appropriate and/or necessary, the patients caregiver. Nor do the ESC Guidelines exempt health professionals from taking full and careful consideration of the relevant official updated recommendations or guidelines issued by competent public health authorities in order to manage each
patients case in the light of the scientifically accepted data pursuant to their respective ethical and professional obligations. It is also the health professionals responsibility to verify the
applicable rules and regulations relating to drugs and medical devices at the time of prescription.
&The European Society of Cardiology 2014. All rights reserved. For permissions please email: journals.permissions@oup.com.
Downloaded from http://eurheartj.oxfordjournals.org/ by guest on August 10, 2014
Authors/Task Force Members: Steen Dalby Kristensen* (Chairperson) (Denmark),

Juhani Knuuti* (Chairperson) (Finland), Antti Saraste (Finland), Stefan Anker
(Germany), Hans Erik Btker (Denmark), Stefan De Hert (Belgium), Ian Ford (UK),
Jose Ramon Gonzalez-Juanatey (Spain), Bulent Gorenek (Turkey),
Guy Robert Heyndrickx (Belgium), Andreas Hoeft (Germany), Kurt Huber (Austria),
Bernard Iung (France), Keld Per Kjeldsen (Denmark), Dan Longrois (France),
Thomas F. Luscher (Switzerland), Luc Pierard (Belgium), Stuart Pocock (UK),
Susanna Price (UK), Marco Roffi (Switzerland), Per Anton Sirnes (Norway),
Miguel Sousa-Uva (Portugal), Vasilis Voudris (Greece), Christian Funck-Brentano
(France).
Page 2 of 49
ESC/ESA Guidelines
ESA Clinical Guidelines Committee: Maurizio Solca (Chairperson) (Italy), Jean-Francois Brichant (Belgium),
Stefan De Hert a, (Belgium), Edoardo de Robertis b, (Italy), Dan Longroisc, (France), Sibylle Kozek Langenecker
(Austria), Josef Wichelewski (Israel).
Document Reviewers: Massimo F. Piepoli (Review co-ordinator) (Italy), William Wijns (Review co-ordinator)
(Belgium), Stefan Agewall (Norway), Claudio Ceconi (Italy), Antonio Coca (Spain), Ugo Corra` (Italy),
Raffaele De Caterina (Italy), Carlo Di Mario (UK), Thor Edvardsen (Norway), Robert Fagard (Belgium),
Giuseppe Germano (Italy), Fabio Guarracino (Italy), Arno Hoes (Netherlands), Torben Joergensen (Denmark),
ztekin Oto (Turkey),
Peter Juni (Switzerland), Pedro Marques-Vidal (Switzerland), Christian Mueller (Switzerland), O
Philippe Pibarot (Canada), Piotr Ponikowski (Poland), Olav FM Sellevold (Norway), Filippos Triposkiadis (Greece),
Stephan Windecker (Switzerland), Patrick Wouters (Belgium).
ESC National Cardiac Societies document reviewers listed in appendix.
The disclosure forms of the authors and reviewers are available on the ESC website www.escardio.org/guidelines
a
Scientific Committee Chairperson & ESA Board Representative; bNASC Chairperson; and cEBA/UEMS representative
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - Keywords
Table of Contents
Abbreviations and acronyms . . . . . . . . . . . . . . . . . . . . . . .
1. Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.1 The magnitude of the problem . . . . . . . . . . . . . . . . .
2.2 Change in demographics . . . . . . . . . . . . . . . . . . . . .
2.3 Purpose and organization . . . . . . . . . . . . . . . . . . . .
3. Pre-operative evaluation . . . . . . . . . . . . . . . . . . . . . . . .
3.1 Surgical risk for cardiac events . . . . . . . . . . . . . . . . .
3.2 Type of surgery . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.1 Endovascular vs. open vascular procedures . . . . . .
3.2.2 Open vs. laparoscopic or thoracoscopic procedures
3.3 Functional capacity. . . . . . . . . . . . . . . . . . . . . . . . .
3.4 Risk indices . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.5 Biomarkers . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.6 Non-invasive testing . . . . . . . . . . . . . . . . . . . . . . . .
3.6.1 Non-invasive testing of cardiac disease . . . . . . . . .
3.6.2 Non-invasive testing of ischaemic heart disease. . . .
3.7 Invasive coronary angiography . . . . . . . . . . . . . . . . .
4. Risk-reduction strategies . . . . . . . . . . . . . . . . . . . . . . . .
4.1 Pharmacological . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.1 Beta-blockers . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.2 Statins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.3 Nitrates. . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.4 Angiotensin-converting enzyme inhibitors and
angiotensin-receptor blockers . . . . . . . . . . . . . . . . . . .
4.1.5 Calcium channel blockers . . . . . . . . . . . . . . . . .
4.1.6 Alpha2 receptor agonists . . . . . . . . . . . . . . . . . .
4.1.7 Diuretics . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2 Peri-operative management in patients on anti-platelet
agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.1 Aspirin . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2.2 Dual anti-platelet therapy . . . . . . . . . . . . . . . . .
4.2.3 Reversal of anti-platelet therapy . . . . . . . . . . . . .
4.3 Peri-operative management in patients on anticoagulants
4.3.1 Vitamin K antagonists . . . . . . . . . . . . . . . . . . . .
4.3.2 Non-vitamin K antagonist oral anticoagulants . . . . .
3
4
5
5
5
5
7
7
7
7
8
8
9
10
10
11
11
13
13
13
13
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4.3.3 Reversal of anticoagulant therapy . . . . . . . . . . . .

4.4 Revascularization. . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.1 Prophylactic revascularization in patients with
asymptomatic or stable ischaemic heart disease . . . . . . . .
4.4.2 Type of prophylactic revascularization in patients
with stable ischaemic heart disease . . . . . . . . . . . . . . . .
4.4.3 Revascularization in patients with non-ST-elevation
acute coronary syndrome . . . . . . . . . . . . . . . . . . . . . .
5. Specific diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.1 Chronic heart failure . . . . . . . . . . . . . . . . . . . . . . .
5.2 Arterial hypertension . . . . . . . . . . . . . . . . . . . . . . .
5.3 Valvular heart disease . . . . . . . . . . . . . . . . . . . . . . .
5.3.1 Patient evaluation . . . . . . . . . . . . . . . . . . . . . .
5.3.2 Aortic stenosis . . . . . . . . . . . . . . . . . . . . . . . .
5.3.3 Mitral stenosis. . . . . . . . . . . . . . . . . . . . . . . . .
5.3.4 Primary aortic regurgitation and mitral regurgitation
5.3.5 Secondary mitral regurgitation . . . . . . . . . . . . . .
5.3.6 Patients with prosthetic valve(s) . . . . . . . . . . . . .
5.3.7 Prophylaxis of infective endocarditis. . . . . . . . . . .
5.4 Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.4.1 New-onset ventricular arrhythmias in the
pre-operative period . . . . . . . . . . . . . . . . . . . . . . . . .
5.4.2 Management of supraventricular arrhythmias and
atrial fibrillation in the pre-operative period. . . . . . . . . . .
5.4.3 Peri-operative bradyarrhythmias . . . . . . . . . . . . .
5.4.4 Peri-operative management of patients with
pacemaker/implantable cardioverter defibrillator . . . . . . .
5.5 Renal disease . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.6 Cerebrovascular disease . . . . . . . . . . . . . . . . . . . . .
5.7 Peripheral artery disease . . . . . . . . . . . . . . . . . . . . .
5.8 Pulmonary disease . . . . . . . . . . . . . . . . . . . . . . . . .
5.9 Congenital heart disease . . . . . . . . . . . . . . . . . . . . .
6. Peri-operative monitoring. . . . . . . . . . . . . . . . . . . . . . . .
6.1 Electrocardiography . . . . . . . . . . . . . . . . . . . . . . . .
6.2 Transoesophageal echocardiography . . . . . . . . . . . . .
6.3 Right heart catheterization. . . . . . . . . . . . . . . . . . . .
20
21
22
23
23
24
24
26
26
26
26
27
27
27
27
27
28
28
28
29
29
29
31
32
33
34
34
34
35
36
Guidelines Non-cardiac surgery Pre-operative cardiac risk assessment Pre-operative cardiac testing
Pre-operative coronary artery revascularization Peri-operative cardiac management Anti-thrombotic
therapy Beta-blockers Valvular disease Arrhythmias Heart failure Renal disease Pulmonary
disease Cerebrovascular disease Anaesthesiology Post-operative cardiac surveillance
Page 3 of 49
ESC/ESA Guidelines
6.4 Disturbed glucose metabolism . . . . . . . . . . .

6.5 Anaemia . . . . . . . . . . . . . . . . . . . . . . . . .
7. Anaesthesia. . . . . . . . . . . . . . . . . . . . . . . . . . .
7.1 Intra-operative anaesthetic management . . . . .
7.2 Neuraxial techniques . . . . . . . . . . . . . . . . .
7.3 Peri-operative goal-directed therapy . . . . . . .
7.4 Risk stratification after surgery . . . . . . . . . . .
7.5 Early diagnosis of post-operative complications
7.6 Post-operative pain management. . . . . . . . . .
8. Gaps in evidence . . . . . . . . . . . . . . . . . . . . . . .
9. Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . .
10. Appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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43
Abbreviations and acronyms
CI
CI-AKI
CKD
CKD-EPI
Cmax
CMR
COPD
CPG
CPX/CPET
CRP
CRT
CRT-D
CT
cTnI
cTnT
CVD
CYP3a4
DAPT
DECREASE
DES
DIPOM
DSE
abdominal aortic aneurysm

angiotensin converting enzyme inhibitor
acute coronary syndromes
atrial fibrillation
acute kidney injury
Acute Kidney Injury Network
angiotensin receptor blocker
American Society of Anesthesiologists
bis in diem (twice daily)
Beta-Blocker in Spinal Anesthesia
bare-metal stent
B-type natriuretic peptide
beats per minute
coronary artery bypass graft
coronary artery disease
Coronary Artery Revascularization Prophylaxis
carotid artery stenting
Coronary Artery Surgery Study
carotid endarterectomy
cardiac failure, hypertension, age 75 (doubled), diabetes, stroke (doubled)-vascular disease, age 6574
and sex category (female)
confidence interval
contrast-induced acute kidney injury
chronic kidney disease
Chronic Kidney Disease Epidemiology Collaboration
maximum concentration
cardiovascular magnetic resonance
chronic obstructive pulmonary disease
Committee for Practice Guidelines
cardiopulmonary exercise test
C-reactive protein
cardiac resynchronization therapy
cardiac resynchronization therapy defibrillator
computed tomography
cardiac troponin I
cardiac troponin T
cardiovascular disease
cytochrome P3a4 enzyme
dual anti-platelet therapy
Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography
drug-eluting stent
DIabetic Post-Operative Mortality and Morbidity
dobutamine stress echocardiography
eGFR
ESA
ESC
EVAR
FEV1
HbA1c
HF-PEF
HF-REF
ICD
ICU
IHD
INR
IOCM
KDIGO
LMWH
LOCM
LV
LVEF
MaVS
MDRD
MET
MRI
NHS
NOAC
NSQIP
NSTE-ACS
NT-proBNP
O2
OHS
OR
P gp
PAC
PAD
PAH
PCC
PCI
POBBLE
POISE
POISE-2
q.d.
RIFLE
SPECT
SVT
SYNTAX
TAVI
TdP
TIA
TOE
TOD
TTE
UFH
VATS
VHD
VISION
VKA
VPB
VT
electrocardiography/electrocardiographically/electrocardiogram
estimated glomerular filtration rate
European Society of Anaesthesiology
European Society of Cardiology
endovascular abdominal aortic aneurysm repair
Forced expiratory volume in 1 second
glycosylated haemoglobin
heart failure with preserved left ventricular ejection fraction
heart failure with reduced left ventricular ejection fraction
implantable cardioverter defibrillator
intensive care unit
ischaemic heart disease
international normalized ratio
iso-osmolar contrast medium
Kidney Disease: Improving Global Outcomes
low molecular weight heparin
low-osmolar contrast medium
left ventricular
left ventricular ejection fraction
Metoprolol after Vascular Surgery
Modification of Diet in Renal Disease
metabolic equivalent
magnetic resonance imaging
National Health Service
non-vitamin K oral anticoagulant
National Surgical Quality Improvement Program
non-ST-elevation acute coronary syndromes
N-terminal pro-BNP
oxygen
obesity hypoventilation syndrome
odds ratio
platelet glycoprotein
pulmonary artery catheter
peripheral artery disease
pulmonary artery hypertension
prothrombin complex concentrate
percutaneous coronary intervention
Peri-Operative Beta-BLockadE
Peri-Operative ISchemic Evaluation
Peri-Operative ISchemic Evaluation 2
quaque die (once daily)
Risk, Injury, Failure, Loss, End-stage renal disease
single photon emission computed tomography
supraventricular tachycardia
Synergy between Percutaneous Coronary Intervention
with TAXUS and Cardiac Surgery
transcatheter aortic valve implantation
torsades de pointes
transient ischaemic attack
transoesophageal echocardiography
transoesophageal doppler
transthoracic echocardiography
unfractionated heparin
video-assisted thoracic surgery
valvular heart disease
Vascular Events In Noncardiac Surgery Patients Cohort
Evaluation
vitamin K antagonist
ventricular premature beat
ventricular tachycardia
AAA
ACEI
ACS
AF
AKI
AKIN
ARB
ASA
b.i.d.
BBSA
BMS
BNP
bpm
CABG
CAD
CARP
CAS
CASS
CEA
CHA2DS2-VASc
ECG
Page 4 of 49
ESC/ESA Guidelines
1. Preamble
Table 1
Classes of recommendations
Classes of
recommendations
Class I
Suggested wording to use

Evidence and/or general agreement
that a given treatment or procedure
Is recommended/is
indicated
Class II
divergence of opinion about the
treatment or procedure.
Class IIa
Class IIb
Class III
Weight of evidence/opinion is in
established by evidence/opinion.
Evidence or general agreement that
the given treatment or procedure
is not useful/effective, and in some
cases may be harmful.
Should be considered
May be considered
Is not recommended
Guidelines summarize and evaluate all available evidence, at the time

of the writing process, on a particular issue with the aim of assisting
health professionals in selecting the best management strategies for
an individual patient with a given condition, taking into account the
impact on outcome, as well as the risk benefit ratio of particular
diagnostic or therapeutic means. Guidelines and recommendations
should help health professionals to make decisions in their daily practice; however, the final decisions concerning an individual patient
must be made by the responsible health professional(s), in consultation with the patient and caregiver as appropriate.
A great number of guidelines have been issued in recent years by the
European Society of Cardiology (ESC) and the European Society of
Anaesthesiology (ESA), as well as by other societies and organisations.
Because of their impact on clinical practice, quality criteria for the development of guidelines have been established in order to make
all decisions transparent to the user. The recommendations for formulating and issuing ESC/ESA Guidelines can be found on the ESC
web site (http://www.escardio.org/guidelines-surveys/esc-guidelines/
about/Pages/rules-writing.aspx). These ESC/ESA guidelines represent
the official position of these two societies on this given topic and are
regularly updated.
Members of this Task Force were selected by the ESC and ESA to
represent professionals involved with the medical care of patients
with this pathology. Selected experts in the field undertook a comprehensive review of the published evidence for management
(including diagnosis, treatment, prevention and rehabilitation) of a
given condition, according to the ESC Committee for Practice
Guidelines (CPG) and ESA Guidelines Committee policy. A critical
evaluation of diagnostic and therapeutic procedures was performed, including assessment of the risk benefit ratio. Estimates
of expected health outcomes for larger populations were included,
where data exist. The level of evidence and the strength of
recommendation of particular management options were

weighed and graded according to pre-defined scales, as outlined
in Tables 1 and 2.
The experts of the writing and reviewing panels completed declarations of interest forms which might be perceived as real or potential
sources of conflicts of interest. These forms were compiled into one
file and can be found on the ESC web site (http://www.escardio.org/
guidelines). Any changes in declarations of interest that arise during
the writing period must be notified to the ESC/ESA and updated.
The Task Force received its entire financial support from the ESC
and ESA, without any involvement from the healthcare industry.
The ESC CPG supervises and co-ordinates the preparation of new
guidelines produced by Task Forces, expert groups or consensus
panels. The Committee is also responsible for the endorsement
process of these guidelines. The ESC and Joint Guidelines undergo
extensive review by the CPG and partner Guidelines Committee
and external experts. After appropriate revisions it is approved by
all the experts involved in the Task Force. The finalized document
is approved by the CPG/ESA for simultaneous publication in the
European Heart Journal and joint partner journal, in this instance
the European Journal of Anaesthesiology. It was developed after
careful consideration of the scientific and medical knowledge and
the evidence available at the time of their dating.
The task of developing ESC/ESA guidelines covers not only the
integration of the most recent research, but also the creation of educational tools and implementation programmes for the recommendations. To implement the guidelines, condensed pocket versions,
summary slides, booklets with essential messages, summary cards
for non-specialists, electronic versions for digital applications
(smart phones etc.) are produced. These versions are abridged and
thus, if needed, one should always refer to the full-text version,
which is freely available on the ESC and ESA web sites. The national
societies of the ESC and of the ESA are encouraged to endorse, translate and implement the ESC guidelines. Implementation programmes
Page 5 of 49
ESC/ESA Guidelines
Table 2
Levels of evidence
Level of
evidence A
Data derived from multiple randomized

clinical trials or meta-analyses.
Level of
evidence B
Data derived from a single randomized

clinical trial or large non-randomized
studies.
Level of
evidence C
Consensus of opinion of the experts and/

or small studies, retrospective studies,
registries.
2. Introduction
2.1 The magnitude of the problem
The present Guidelines focus on the cardiovascular management of
patients in whom heart disease is a potential source of complications
during non-cardiac surgery. The risk of peri-operative complications
depends on the condition of the patient before surgery, the prevalence of comorbidities, and the urgency, magnitude, type, and duration of the surgical procedure.
More specifically, cardiac complications can arise in patients with
documented or asymptomatic ischaemic heart disease (IHD), left
ventricular (LV) dysfunction, valvular heart disease (VHD), and
arrhythmias, who undergo surgical procedures that are associated
with prolonged haemodynamic and cardiac stress. In the case of perioperative myocardial ischaemia, two mechanisms are important: (i) a
mismatch in the supply demand ratio of blood flow, in response to
metabolic demand due to a coronary artery stenosis that may
become flow-limiting by peri-operative haemodynamic fluctuations
and (ii) acute coronary syndromes (ACS) due to stress-induced
rupture of a vulnerable atherosclerotic plaque in combination with
vascular inflammation and altered vasomotion, as well as haemostasis. LV dysfunction and arrhythmias may occur for various reasons at
all ages. Because the prevalence of not only IHD but also VHD and
arrhythmias increases with age, peri-operative cardiac mortality
and morbidity are predominantly an issue in the adult population

undergoing major non-cardiac surgery.
The magnitude of the problem in Europe can best be understood in
terms of (i) the size of the adult non-cardiac surgical group and (ii) the
average risk of cardiac complications in this cohort. Unfortunately,
systematic data on the annual number and type of operationsand
on patient outcomesare only available at a national level in 23
European countries (41%).1 Additionally, data definitions vary, as
do data quantity and quality. A recent modelling strategy, based on
worldwide data available in 2004, estimated the number of major
operations to be at the rate of 4% of the world population per
year.1 When applied to Europe, with an overall population of over
500 million, this figure translates into a crude estimate of 19 million
major procedures annually. While the majority of these procedures
are performed in patients with minimal cardiovascular risk, 30% of
patients undergo extensive surgical procedures in the presence of
cardiovascular comorbidity; hence, 5.7 million procedures annually
are performed in European patients who present with increased
risk of cardiovascular complications.
Worldwide, non-cardiac surgery is associated with an average
overall complication rate of 7 11% and a mortality rate of 0.8
1.5%, depending on safety precautions.2 Up to 42% of these are
caused by cardiac complications.3 When applied to the population
in the European Union member states, these figures translate into
at least 167 000 cardiac complications annually due to non-cardiac
surgical procedures, of which 19 000 are life-threatening.
2.2 Change in demographics

Within the next 20 years, the ageing of the population will have a
major impact on peri-operative patient management. It is estimated
that elderly people require surgery four times as often than the
rest of the population.4 In Europe, it is estimated that the number
of patients undergoing surgery will increase by 25% by 2020. Over
the same time period, the elderly population will increase by 50%.
The total number of surgical procedures may increase even faster
because of the rising frequency of interventions with age.5 The
results of the United States National Hospital Discharge Survey
show that the number of surgical procedures will increase in
almost all age groups and that the largest increase will occur in the
middle-aged and elderly. Demographics of patients undergoing
surgery show a trend towards an increasing number of elderly
patients and comorbidities.6 Although mortality from cardiac
disease is decreasing in the general population, the prevalence of
IHD, heart failure, and cardiovascular risk factorsespecially diabetesis increasing. Among the significant comorbidities in elderly
patients presenting for general surgery, cardiovascular disease
(CVD) is the most prevalent.7 Age per se, however, seems to be responsible for only a small increase in the risk of complications;
greater risks are associated with urgency and significant cardiac, pulmonary, and renal disease; thus, these conditions should have greater
impact on the evaluation of patient risk than age alone.
2.3 Purpose and organization

These Guidelines are intended for physicians and collaborators
involved in the pre-operative, operative, and post-operative care of
patients undergoing non-cardiac surgery.
are needed because it has been shown that the outcome of disease
may be favourably influenced by the thorough application of clinical
recommendations.
Surveys and registries are needed to verify that real-life daily practice is in keeping with what is recommended in the guidelines, thus
completing the loop between clinical research, writing of guidelines,
disseminating them and implementing them into clinical practice.
Health professionals are encouraged to take the ESC/ESA guidelines fully into account when exercising their clinical judgment, as
well as in the determination and the implementation of preventive,
diagnostic or therapeutic medical strategies; however, the ESC/ESA
guidelines do not, in any way whatsoever, override the individual responsibility of health professionals to make appropriate and accurate
decisions in consideration of the condition of each patients health
and in consultation with that patient and, where appropriate
and/or necessary, the patients caregiver. It is also the health professionals responsibility to verify the rules and regulations applicable to
drugs and devices at the time of prescription.
Page 6 of 49
Table 3
ESC/ESA Guidelines
Surgical risk estimate according to type of surgery or interventiona,b
CAS carotid artery stenting; CEA carotid endarterectomy.

a
Surgical risk estimate is a broad approximation of 30-day risk of cardiovascular death and myocardial infarction that takes into account only the specific surgical intervention, without
considering the patients comorbidities.
b
Adapted from Glance et al. 11
both began the process of revising their respective guidelines concurrently. The respective writing committees independently performed
their literature review and analysis, and then developed their recommendations. Once peer review of both guidelines was completed, the
writing committees chose to discuss their respective recommendations regarding beta-blocker therapy and other relevant issues. Any
differences in recommendations were discussed and clearly articulated in the text; however, the writing committees aligned a few
recommendations to avoid confusion within the clinical community,
except where international practice variation was prevalent.
Following the development and introduction of peri-operative
cardiac guidelines, their effect on outcome should be monitored.
The objective evaluation of changes in outcome will form an essential
part of future peri-operative guideline development.
Recommendations on pre-operative evaluation
Recommendations
Selected patients with cardiac
disease undergoing low-and
intermediate-risk non-cardiac
surgery may be referred by
the anaesthesiologist for
cardiological evaluation and
medical optimization.
A multidisciplinary expert
team should be considered for
pre-operative evaluation of
patients with known or high
risk of cardiac disease
undergoing high-risk noncardiac surgery.
a
Class of recommendation.
Level of evidence.
c
Reference(s) supporting recommendations.
b
Classa
Levelb
IIb
IIa
Ref. c
The objective is to endorse a standardized and evidence-based approach to peri-operative cardiac management. The Guidelines recommend a practical, stepwise evaluation of the patient that integrates
clinical risk factors and test results with the estimated stress of the
planned surgical procedure. This results in an individualized cardiac
risk assessment, with the opportunity of initiating medical therapy, coronary interventions, and specific surgical and anaesthetic techniques in
order to optimize the patients peri-operative condition.
Compared with the non-surgical setting, data from randomized
clinical trialswhich provide the ideal evidence-base for the guidelinesare sparse. Consequently, when no trials are available on a
specific cardiac-management regimen in the surgical setting, data
from the non-surgical setting are extrapolated and similar recommendations made, but with different levels of evidence. Anaesthesiologists, who are experts on the specific demands of the proposed
surgical procedure, will usually co-ordinate the pre-operative evaluation. The majority of patients with stable heart disease can undergo
low and intermediate-risk surgery (Table 3) without additional evaluation. Selected patients require evaluation by a team of integrated
multidisciplinary specialists including anaesthesiologists, cardiologists, and surgeons and, when appropriate, an extended team (e.g.
internists, intensivists, pulmonologists or geriatricians).8 Selected
patients include those identified by the anaesthesiologist because
of suspected or known cardiac disease with sufficient complexity
to carry a potential peri-operative risk (e.g. congenital heart
disease, unstable symptoms or low functional capacity), patients in
whom pre-operative medical optimization is expected to reduce
peri-operative risk before low- and intermediate-risk surgery, and
patients with known or high risk of cardiac disease who are undergoing high-risk surgery. Guidelines have the potential to improve postoperative outcomes and highlight the existence of a clear opportunity
for improving the quality of care in this high-risk group of patients. In
addition to promoting an improvement in immediate peri-operative
care, guidelines should provide long-term advice.
Because of the availability of new evidence and the international
impact of the controversy over the DECREASE trials, the ESC/ESA
and American College of Cardiology/American Heart Association
Page 7 of 49
ESC/ESA Guidelines
3. Pre-operative evaluation
3.1 Surgical risk for cardiac events
3.2 Type of surgery

In general, endoscopic and endovascular techniques speed recovery,
decrease hospital stay, and reduce the rate of complications.12
However, randomized clinical trials comparing laparoscopic with
open techniques exclude older, sicker, and urgent patients, and
results from an expert-based randomized trial (laparoscopic vs.
open cholecystectomy) have shown no significant differences in
conversion rate, pain, complications, length of hospital stay, or
re-admissions.13
The wide variety of surgical procedures, in a myriad of different
contexts, makes difficult the assignation of a specific risk of a
major adverse cardiac event to each procedure. When alternative
methods to classical open surgery are considered, either through
endovascular or less-invasive endoscopic procedures, the
potential trade-offs between early benefits due to reduced
morbidity and mid- to long-term efficacy need to be taken into
account.
3.2.1 Endovascular vs. open vascular procedures
Vascular interventions are of specific interest, not only because they
carry the highest risk of cardiac complications, but also because of
the many studies that have shown that this risk can be influenced
by adequate peri-operative measures in these patients.14 Open
aortic and infra-inguinal procedures must both be regarded as highrisk procedures. Although it is a less-extensive intervention, infrainguinal revascularization entails a cardiac risk similar toor even
higher thanthat of aortic procedures. This can be explained
by the higher incidence of diabetes, renal dysfunction, IHD, and
advanced age in this patient group. This also explains why the risk
related to peripheral artery angioplasties, which are minimally invasive procedures, is not negligible.
Endovascular AAA repair (EVAR) has been associated with
lower operative mortality and morbidity than open repair but this
advantage reduces with time, due to more frequent graft-related
complications and re-interventions in patients who underwent
EVAR, resulting in similar long-term AAA-related mortality and
total mortality.15 17
A meta-analysis of studies, comparing open surgical with
percutaneous transluminal methods for the treatment of femoropopliteal arterial disease, showed that bypass surgery is associated
with higher 30-day morbidity [odds ratio (OR) 2.93; 95%
confidence interval (CI) 1.34 6.41] and lower technical failure
than endovascular treatment, with no differences in 30-day mortality; however, there were higher amputation-free and overall
survival rates in the bypass group at 4 years.18 Therefore, multiple
factors must be taken into consideration when deciding which
type of procedure serves the patient best. An endovascular-first approach may be advisable in patients with significant comorbidity,
whereas a bypass procedure may be offered as a first-line interventional treatment for fit patients with a longer life expectancy.19
Carotid artery stenting has appeared as an attractive, less-invasive
alternative to CEA; however, although CAS reduces the rate of
Cardiac complications after non-cardiac surgery depend on

patient-related risk factors, on the type of surgery, and on the circumstances under which it takes place.9 Surgical factors that influence cardiac risk are related to the urgency, invasiveness, type,
and duration of the procedure, as well as the change in body core
temperature, blood loss, and fluid shifts.5 Every operation elicits a
stress response. This response is initiated by tissue injury and
mediated by neuro-endocrine factors, and may induce sympathovagal imbalance. Fluid shifts in the peri-operative period add to
the surgical stress. This stress increases myocardial oxygen
demand. Surgery also causes alterations in the balance between
prothrombotic and fibrinolytic factors, potentially resulting in
increased coronary thrombogenicity. The extent of such changes
is proportionate to the extent and duration of the intervention.
These factors, together with patient position, temperature
management, bleeding, and type of anaesthesia, may contribute to
haemodynamic derangements, leading to myocardial ischaemia
and heart failure. General, locoregional, and neuraxial anaesthesia
differ in terms of the stress response evoked by surgery. Less
invasive anaesthetic techniques may reduce early mortality in
patients at intermediate-to-high cardiac risk and limit postoperative complications.10 Although patient-specific factors are
more important than surgery-specific factors in predicting the
cardiac risk for non-cardiac surgical procedures, the type of
surgery cannot be ignored.9
With regard to cardiac risk, surgical interventionswhich include
open or endovascular procedurescan be broadly divided into
low-risk, intermediate-risk, and high-risk groups, with estimated
30-day cardiac event rates (cardiac death and myocardial infarction)
of ,1%, 1 5%, and .5%, respectively (Table 3).
The need for, and value of, pre-operative cardiac evaluation will
also depend on the urgency of surgery. In the case of emergency surgical procedures, such as those for ruptured abdominal aortic aneurysm (AAA), major trauma, or for a perforated viscus, cardiac
evaluation will not alter the course or result of the intervention but
may influence management in the immediate peri-operative period.
In non-emergency but urgent surgical conditions, such as bypass
for acute limb ischaemia or treatment of bowel obstruction, the morbidity and mortality of the untreated underlying condition may outweigh the potential cardiac risk related to the intervention. In these
cases, cardiological evaluation may influence the peri-operative measures taken to reduce cardiac risk but will not influence the decision
to perform the intervention. In some cases, the cardiac risk can also
influence the type of operation and guide the choice to less-invasive
interventions, such as peripheral arterial angioplasty instead of infra-inguinal bypass, or extra-anatomical reconstruction instead of
an aortic procedure, even when these may yield less favourable
results in the long term. Finally, in some situations, the cardiac evaluation (in as far as it can reliably predict peri-operative cardiac complications and late survival) should be taken into consideration when
deciding whether to perform an intervention or manage conservatively. This is the case in certain prophylactic interventions, such as
the treatment of small AAAs or asymptomatic carotid stenosis,
where the life expectancy of the patient and the risk of the operation are important factors in evaluating the potential benefit of the
surgical intervention.
Page 8 of 49
periprocedural myocardial infarction and cranial nerve palsy, the
combined 30-day rate of stroke or death is higher than CEA,
particularly in symptomatic and older patients, driven by a difference in the risk of periprocedural non-disabling stroke.20,21
The benefit of carotid revascularization is particularly high in
patients with recent (,3 months) transient ischaemic attack
(TIA) or stroke and a .60% carotid artery bifurcation stenosis.22
In neurologically asymptomatic patients, carotid revascularization
benefit is questionable, compared with modern medical
therapy, except in patients with a .80% carotid stenosis and an
estimated life expectancy of .5 years.21 The choice between
CEA and CAS must integrate operator experience and results,
anatomical characteristics of the arch vessels, neck features, and
comorbidities.21 23
Recommendations on the selection of surgical approach

and its impact on risk
Recommendations
Classa
Levelb
Ref.c
It is recommended that patients

should undergo pre-operative risk
assessment independently of an
open or laparoscopic surgical
approach.d
26,27,
35
In patients with AAA 55 mm,

anatomically suited for EVAR,
either open or endovascular aortic
repair is recommended if surgical
risk is acceptable.
1517
In patients with asymptomatic

AAA who are unfit for open
repair, EVAR, along with best
medical treatment, may be
considered.
IIb
15,35
In patients with lower extremity

artery disease requiring
revascularization, the best
management strategy should be
determined by an expert team
considering anatomy,
comorbidities, local availability, and
expertise.
IIa
18
AAA abdominal aortic aneurysm; EVAR endovascular aortic reconstruction.

a
b
Level of evidence.
c
d
Since laparoscopic procedures demonstrate a cardiac stress similar to that of open
procedures.
3.3 Functional capacity

Determination of functional capacity is a pivotal step in preoperative cardiac risk assessment and is measured in metabolic
equivalents (METs). One MET equals the basal metabolic rate. Exercise testing provides an objective assessment of functional capacity. Without testing, functional capacity can be estimated from
the ability to perform the activities of daily living. One MET represents metabolic demand at rest; climbing two flights of stairs
demands 4 METs, and strenuous sports, such as swimming, .10
METS (Figure 1).
The inability to climb two flights of stairs or run a short distance
(,4 METs) indicates poor functional capacity and is associated
with an increased incidence of post-operative cardiac events. After
thoracic surgery, a poor functional capacity has been associated
with an increased mortality (relative risk 18.7; 95% CI 5.9 59);
however, in comparison with thoracic surgery, a poor functional
status was not associated with an increased mortality after other noncardiac surgery (relative risk 0.47; 95% CI 0.092.5).38 This may
3.2.2 Open vs. laparoscopic or thoracoscopic

procedures
Laparoscopic procedures, compared with open procedures, have
the advantage of causing less tissue trauma and intestinal paralysis,
resulting in less incisional pain, better post-operative pulmonary
function, significantly fewer wall complications, and diminished postoperative fluid shifts related to bowel paralysis.24 However, the pneumoperitoneum required for these procedures results in elevated
intra-abdominal pressure and a reduction in venous return. Typical
physiological sequelae are secondary to increased intra-abdominal
pressure and absorption of the gaseous medium used for insufflation.
While healthy individuals on controlled ventilation typically tolerate
pneumoperitoneum, debilitated patients with cardiopulmonary
compromise and obese patients may experience adverse consequences.25 Pneumoperitoneum and Trendelenburg position result
in increased mean arterial pressure, central venous pressure, mean
pulmonary artery, pulmonary capillary wedge pressure, and systemic
vascular resistance impairing cardiac function.26,27 Therefore, compared with open surgery, cardiac risk in patients with heart failure
is not reduced in patients undergoing laparoscopy, and both should
be evaluated in the same way. This is especially true in patients undergoing interventions for morbid obesity, but also in other types of
surgery, considering the risk of conversion to an open procedure.28,29 Superior short-term outcomes of laparoscopic vs. open
procedures have been reported, depending on type of surgery, operator experience and hospital volume, but few studies provide direct
measures of cardiac complications.30 32 Benefit from laparoscopic
procedures is probably greater in elderly patients, with reduced
length of hospital stay, intra-operative blood loss, incidence of postoperative pneumonia, time to return of normal bowel function, incidence of post-operative cardiac complications, and wound infections.33 Few data are available for video-assisted thoracic surgery
(VATS), with no large, randomized trial comparing VATS with
open thoracic lung resection. In one study involving propensityscore-matched patients, VATS lobectomy was associated with no
significant difference in mortality, but with significantly lower
rates of overall peri-operative morbidity, pneumonia, and atrial
arrhythmia.34
ESC/ESA Guidelines
Page 9 of 49
ESC/ESA Guidelines
Functional capacity
1 MET
Can you...
Take care of yourself?
Eat, dress,
or use the toilet?
Walk indoors
around
the house?
Walk 100 m
on level ground
at 3 to 5 km per h?
4 METs
Can you...
4 METs
Climb two flights of stairs

or walk up a hill?
Do heavy work
around the house like
scrubbing floors of lifting
or moving heavy
furniture?
Participate in strenuous
sports like swimming,
singles tennis, football,
basketball, or skiing?
Greater than 10 METs
Based on Hlatky et al. and Fletcher et al. 36,37 km per h kilometres

per hour; MET metabolic equivalent.
reflect the importance of pulmonary functionstrongly related to

functional capacityas a major predictor of survival after thoracic
surgery. These findings were confirmed in a study of 5939 patients
scheduled for non-cardiac surgery, in which the pre-operative functional capacity measured in METs showed a relatively weak association with post-operative cardiac events or death.39 Notably, when
functional capacity is high, the prognosis is excellent, even in the presence of stable IHD or risk factors;40 otherwise, when functional capacity is poor or unknown, the presence and number of risk factors in
relation to the risk of surgery will determine pre-operative risk stratification and peri-operative management.
3.4 Risk indices

For two main reasons, effective strategies aimed at reducing the
risk of peri-operative cardiac complications should involve cardiac
evaluation, using medical history before the surgical procedure,.
Firstly, patients with an anticipated low cardiac riskafter thorough
evaluationcan be operated on safely without further delay. It is
unlikely that risk-reduction strategies will further reduce the
peri-operative risk. Secondly, risk reduction by pharmacological
treatment is most cost-effective in patients with a suspected
increased cardiac risk. Additional non-invasive cardiac imaging techniques are tools to identify patients at higher risk; however, imaging
techniques should be reserved for those patients in whom test
results would influence and change management. Clearly, the intensity of the pre-operative cardiac evaluation must be tailored to the
patients clinical condition and the urgency of the circumstances
requiring surgery. When emergency surgery is needed, the evaluation must necessarily be limited; however, most clinical circumstances allow the application of a more extensive, systematic
approach, with cardiac risk evaluation that is initially based on clinical
Figure 1 Estimated energy requirements for various activities.
characteristics and type of surgery and then extended, if indicated, to

resting electrocardiography (ECG), laboratory measurements, or
other non-invasive assessments.
Several risk indices have been developed during the past 30 years,
based on multivariate analyses of observational data, which
represent the relationship between clinical characteristics and perioperative cardiac mortality and morbidity. The indices developed
by Goldman et al. (1977),41 Detsky et al. (1986),42 and Lee et al.
(1999)43 have become well-known.
Although only a rough estimation, the older risk-stratification
systems may represent useful clinical tools for physicians in respect
of the need for cardiac evaluation, drug treatment, and assessment
of risk for cardiac events. The Lee index or revised cardiac risk
index, a modified version of the original Goldman index, was designed
to predict post-operative myocardial infarction, pulmonary oedema,
ventricular fibrillation or cardiac arrest, and complete heart block.
This risk index comprises six variables: type of surgery, history
of IHD, history of heart failure, history of cerebrovascular disease,
pre-operative treatment with insulin, and pre-operative creatinine
.170 mmol/L (.2 mg/dL), and used to be considered by many clinicians and researchers to be the best currently available cardiac-risk
prediction index in non-cardiac surgery.
All of the above-mentioned risk indices were, however, developed
years ago and many changes have since occurred in the treatment of
IHD and in the anaesthetic, operative and peri-operative management of non-cardiac surgical patients. A new predictive model was recently developed to assess the risk of intra-operative/post-operative
myocardial infarction or cardiac arrest, using the American College of
Surgeons National Surgical Quality Improvement Program (NSQIP)
database.44 This NSQIP MICA model was built on the 2007 data set,
based on patients from 180 hospitals, and was validated with the
2008 data set, both containing .200 000 patients and having predictability. The primary endpoint was intra-operative/post-operative
myocardial infarction or cardiac arrest up to 30 days after surgery.
Five predictors of peri-operative myocardial infarction/cardiac
arrest were identified: type of surgery, functional status, elevated creatinine (.130 mmol/L or .1.5 mg/dL), American Society of
Anesthesiologists (ASA) class (Class I, patient is completely healthy;
Class II, patient has mild systemic disease; Class III, patient has
severe systemic disease that is not incapacitating; Class IV, patient
has incapacitating disease that is a constant threat to life; and Class
V, a moribund patient who is not expected to live for 24 hours,
with or without the surgery), and age. This model is presented as
an interactive risk calculator (http://www.surgicalriskcalculator.
com/miorcardiacarrest) so that the risk can be calculated at the
bedside or clinic in a simple and accurate way. Unlike other risk
scores, the NSQIP model did not establish a scoring system but provides a model-based estimate of the probability of myocardial infarction/cardiac arrest for an individual patient. The risk calculator
performed better than the Lee risk index, with some reduction in
performance in vascular patients, although it was still superior;
however, some peri-operative cardiac complications of interest to
clinicians, such as pulmonary oedema and complete heart block,
were not considered in the NSQIP model because those variables
were not included in the NSQIP database. By contrast, the Lee
index allows estimation of the risk of peri-operative pulmonary
Page 10 of 49
oedema and of complete heart block, in addition to death and myocardial infarction (http://www.mdcalc.com/revised-cardiac-riskindex-for-pre-operative-risk/). A recent systematic review of 24
studies covering .790 000 patients found that the Lee index discriminated moderately well patients at low vs. high risk for cardiac
events after mixed non-cardiac surgery, but its performance was
hampered when predicting cardiac events after vascular non-cardiac
surgery or predicting death.45 Therefore, the NSQIP and Lee risk
index models provide complementary prognostic perspectives and
can help the clinician in the decision-making process.
Risk models do not dictate management decisions but should be
regarded as one piece of the puzzle to be evaluated, in concert
with the more traditional information at the physicians disposal.
3.5 Biomarkers
Recommendations on cardiac risk stratification

Classa
Levelb
Ref. c
Clinical risk indices are

recommended to be used
for peri-operative risk
stratification.
43,44
The NSQIP model or the

Lee risk index are
recommended for cardiac
peri-operative risk
stratification.
43,44,54
Assessment of cardiac
troponins in high-risk
patients, both before and
4872 hours after major
surgery, may be
considered.
IIb
3,48,49
NT-proBNP and BNP

measurements may be
considered for obtaining
independent prognostic
information for perioperative and late cardiac
events in high-risk
patients.
IIb
52,53,55
Universal pre-operative
routine biomarker
sampling for risk
stratification and to
prevent cardiac events is
not recommended.
III
Recommendations
BNP B-type natriuretic peptide; NT-proBNP N-terminal pro-brain natriuretic

peptide.
NSQIP National Surgical Quality Improvement Program.
a
b
Level of evidence.
c
3.6 Non-invasive testing

Pre-operative non-invasive testing aims to provide information on
three cardiac risk markers: LV dysfunction, myocardial ischaemia,
and heart valve abnormalities, all of which are major determinants
of adverse post-operative outcome. LV function is assessed at rest,
and various imaging methods are available. For detection of myocardial ischaemia, exercise ECG and non-invasive imaging techniques
may be used. Routine chest X-ray before non-cardiac surgery is
not recommended without specific indications. The overall theme
is that the diagnostic algorithm for risk stratification of myocardial ischaemia and LV function should be similar to that proposed for
patients in the non-surgical setting with known or suspected
IHD.56 Non-invasive testing should be considered not only for coronary artery revascularization but also for patient counselling,
change of peri-operative management in relation to type of
surgery, anaesthetic technique, and long-term prognosis.
A biological marker, or biomarker, is a characteristic that can be objectively measured and which is an indicator of biological processes.
In the peri-operative setting, biomarkers can be divided into markers
focusing on myocardial ischaemia and damage, inflammation, and LV
function. Cardiac troponins T and I (cTnT and cTnI, respectively) are
the preferred markers for the diagnosis of myocardial infarction
because they demonstrate sensitivity and tissue specificity better
than other available biomarkers.46 The prognostic information is independent ofand complementary toother important cardiac
indicators of risk, such as ST deviation and LV function. It seems
that cTnI and cTnT are of similar value for risk assessment in ACS
in the presence and absence of renal failure. Existing evidence suggests that even small increases in cTnT in the peri-operative period
reflect clinically relevant myocardial injury with worsened cardiac
prognosis and outcome.47 49 The development of new biomarkers,
including high-sensitivity troponins, will probably further enhance the
assessment of myocardial damage.48 Assessment of cardiac troponins in high-risk patients, both before and 48 72 hours after major
surgery, may therefore be considered.3 It should be noted that troponin elevation may also be observed in many other conditions; the
diagnosis of non-ST-segment elevation myocardial infarction
should never be made solely on the basis of biomarkers.
Inflammatory markers might pre-operatively identify those
patients with an increased risk of unstable coronary plaque;
however, in the surgical setting, no data are currently available on
how inflammatory markers would alter risk-reduction strategies.
B-type natriuretic peptide (BNP) and N-terminal pro-BNP
(NT-proBNP) are produced in cardiac myocytes in response to
increases in myocardial wall stress. This may occur at any stage of
heart failure, independently of the presence or absence of myocardial
ischaemia. Plasma BNP and NT-proBNP have emerged as important
prognostic indicators across many cardiac diseases in non-surgical
settings.50 Pre-operative BNP and NT-proBNP levels have additional
prognostic value for long-term mortality and for cardiac events after
major non-cardiac vascular surgery.51 53
Data from prospective, controlled trials on the use of preoperative biomarkers are sparse. Based on the existing data, assessment of serum biomarkers for patients undergoing non-cardiac
surgery cannot be proposed for routine use, but may be considered
in high-risk patients (METs 4 or with a revised cardiac risk index
value .1 for vascular surgery and .2 for non-vascular surgery).
ESC/ESA Guidelines
Page 11 of 49
ESC/ESA Guidelines
3.6.1 Non-invasive testing of cardiac disease

3.6.1.1 Electrocardiography
The 12-lead ECG is commonly performed as part of pre-operative
cardiovascular risk assessment in patients undergoing non-cardiac
surgery. In IHD patients, the pre-operative ECG offers important
prognostic information and is predictive of long-term outcome, independent of clinical findings and peri-operative ischaemia.57 However,
the ECG may be normal or non-specific in patients with myocardial
ischaemia or even with infarction.
Recommendations on routine pre-operative ECG
Recommendations
Class a
Pre-operative ECG may be

considered for patients who have
risk factor(s) and are scheduled for
low-risk surgery.
IIb
Pre-operative ECG may be

considered for patients who have
no risk factors, are above 65 years
of age, and are scheduled for
intermediate-risk surgery.
IIb
Routine pre-operative ECG is not

recommended for patients who
have no risk factors and are
scheduled for low-risk surgery.
III
Ref.c
57
71
ECG electrocardiography.
a
b
Level of evidence.
c
d
Clinical risk factors in Table 4.
3.6.1.2 Assessment of left ventricular function

Resting LV function can be evaluated before non-cardiac surgery
by radionuclide ventriculography, gated single photon emission
Recommendations on resting echocardiography in
asymptomatic patients without signs of cardiac disease
or electrocardiographic abnormalities
Classa
Level b
Rest echocardiography may be

considered in patients undergoing
high-risk surgery.
IIb
Routine echocardiography is not

recommended in patients
undergoing intermediate- or lowrisk surgery.
III
Recommendations
Level of evidence.
3.6.2 Non-invasive testing of ischaemic heart disease

Physical exercise, using a treadmill or bicycle ergometer, provides an
estimate of functional capacity, evaluates blood pressure and heart
rate response, and detects myocardial ischaemia through
ST-segment changes. The accuracy of exercise ECG varies significantly among studies.56 Risk stratification with an exercise test is
not suitable for patients with limited exercise capacity, owing to
their inability to reach their target heart rate. Also, pre-existing
ST-segment abnormalities at restespecially in precordial leads
V5 and V6hamper reliable ST-segment analysis. A gradient of severity in the test result relates to the peri-operative outcome: the
onset of a myocardial ischaemic response at low exercise workloads
is associated with a significantly increased risk of peri-operative and
long-term cardiac events. In contrast, the onset of myocardial ischaemia at high workloads is associated with only a minor risk increase,
but higher than a totally normal test. Pharmacological stress testing
with either nuclear perfusion imaging or echocardiography is more
suitable in patients with limited exercise tolerance.
The role of myocardial perfusion imaging for pre-operative risk
stratifications is well established. In patients with limited exercise capacity, pharmacological stress (dipyridamole, adenosine, or dobutamine) is an alternative stressor. Studies are performed both during
stress and at rest, to determine the presence of reversible defects,
reflecting jeopardized ischaemic myocardium or fixed defects,
reflecting scar or non-viable tissue.
The prognostic value of the extent of ischaemic myocardium, using
semi-quantitative dipyridamole myocardial perfusion imaging, has
been investigated in a meta-analysis of patients undergoing vascular
surgery.60 Study endpoints were peri-operative cardiac death and
myocardial infarction. The authors included nine studies, totalling
1179 patients undergoing vascular surgery, with a 7% 30-day event
rate. In this analysis, reversible ischaemia in ,20% of the LV myocardium did not alter the likelihood of peri-operative cardiac events, compared with those without ischaemia. Patients with more extensive
reversible defects from 2050% were at increased risk.
A second meta-analysis pooled the results of 10 studies evaluating
dipyridamole thallium-201 imaging in candidates for vascular surgery
over a 9-year period from 1985 to 1994.61 The 30-day cardiac death
or non-fatal myocardial infarction rates were 1% in patients with
normal test results, 7% in patients with fixed defects, and 9% in
patients with reversible defects on thallium-201 imaging. Moreover,
three of the 10 studies analysed used semi-quantitative scoring, demonstrating a higher incidence of cardiac events in patients with two or
more reversible defects.
Pre-operative ECG is
recommended for patients who
have risk factor(s)d and are
scheduled for intermediate- or
high-risk surgery.
Level b
computed tomography (SPECT), echocardiography, magnetic resonance imaging (MRI) or multislice computed tomography (CT), all
with similar accuracy. Echocardiography is the most readily available
and versatile tool for evaluating ventricular function. Routine echocardiography is not recommended for the pre-operative evaluation
of ventricular function but may be performed in asymptomatic
patients with high surgical risk.58 Pre-operative LV systolic dysfunction, moderate-to-severe mitral regurgitation, and increased aortic
valve gradients are associated with major cardiac events.59 The
limited predictive value of LV function assessment for peri-operative
outcome may be related to the failure to detect severe underlying
IHD.
Page 12 of 49
Table 4 Clinical risk factors according to the revised

cardiac risk index43
According to the universal definition of myocardial infarction.49
detected during stress and at rest.66 Its accuracy in assessment

of ischaemia is high, with a sensitivity of 83% and a specificity of
86% when wall motion is used (14 studies; 754 patients). When perfusion is assessed (24 studies; 1516 patients), its sensitivity was 91%
and specificity 81%. When evaluated prospectively in a multicentre
study, the sensitivity was 67% and the specificity was 61%.67 There
are limited data on CMR in the pre-operative setting; in one study
dobutamine stress CMR was used in 102 patients undergoing
major non-cardiac surgery; in multivariate analysis, myocardial ischaemia was the strongest predictor of peri-operative cardiac
events (death, myocardial infarction, and heart failure).68 Currently
no data are available in the setting of pre-operative risk stratification.
Computed tomography can be used to detect coronary
calcium, which reflects coronary atherosclerosis, and CT angiography is useful for excluding coronary artery disease (CAD) in
patients who are at low risk of atherosclerosis.69 Currently, no data
are available in the setting of pre-operative risk stratification. All
the various imaging tests have their intrinsic risks and these need to
be taken into account when they are used.70
Recommendations on imaging stress testing before
surgery in asymptomatic patients
Recommendations
Classa
Levelb
IIb
III
Imaging stress testing is recommended

before high-risk surgery in patients with
more than two clinical risk factors and
poor functional capacity (<4 METs).c
Imaging stress testing may be considered
before high- or intermediate-risk
surgery in patients with one or two
clinical risk factors and poor functional
capacity (<4 METs).c
Imaging stress testing is not
recommended before low-risk surgery,
regardless of the patients clinical risk.
MET metabolic equivalent
a
b
Level of evidence.
c
Clinical risk factors in Table 4.
How can these data contribute to a practical algorithm? Testing

should only be performed if its results might influence peri-operative
management. Patients with extensive stress-induced ischaemia represent a high-risk population in whom standard medical therapy
appears insufficient to prevent a peri-operative cardiac event. Preoperative testing is recommended in the case of high-risk surgery
in patients with poor functional capacity (,4 METS) and more
than two of the clinical risk factors listed in Table 4, but may also be
considered in patients with fewer than three of these risk factors. Importantly, pre-operative testing might delay surgery. A similar recommendation is made for intermediate-risk surgery patients, although
no data from randomized trials are available. Considering the low
event rate of patients scheduled for low-risk surgery, it is unlikely
that test results will alter peri-operative management in stable
cardiac patients.
Overall, the positive predictive value of reversible defects for perioperative death or myocardial infarction has decreased in more
recent studies. This is probably related to changes in peri-operative
management and surgical procedures; however, because of the
high sensitivity of nuclear imaging studies for detecting IHD, patients
with a normal scan have an excellent prognosis.
Stress echocardiography using exercise or pharmacological
(dobutamine, dipyridamole) stress has been widely used for preoperative cardiac risk evaluation. The test combines information on
LV function at rest, heart valve abnormalities, and the presence and
extent of stress-inducible ischaemia.62 In one study, 530 patients
were enrolled to evaluate the incremental value of dobutamine
stress echocardiography (DSE) for the assessment of cardiac risk
before non-vascular surgery.63 Multivariate predictors of postoperative events in patients with ischaemia were found to be a
history of heart failure (OR 4.7; 95% CI 1.6 14.0) and ischaemic
threshold ,60% of age-predicted maximal heart rate (OR 7.0; 95%
CI 2.8 17.6). DSE has some limitations: it should not, for example,
be used in patients with severe arrhythmias, significant hypertension,
large thrombus-laden aortic aneurysms, or hypotension.
In general, stress echocardiography has a high negative predictive
value and a negative test is associated with a very low incidence of
cardiac events in patients undergoing surgery; however, the positive
predictive value is relatively low (between 25% and 45%); this means
that the postsurgical probability of a cardiac event is low, despite wall
motion abnormality detection during stress echocardiography.
A negative DSE, performed before scheduled aortic surgery, does
not, however, rule out post-operative myocardial necrosis.64 Failure
to achieve target heart rate is not uncommon, despite an aggressive
DSE regimen. A negative DSE without resting wall motion abnormalities has excellent negative predictive value, regardless of the heart
rate achieved. Patients with resting wall motion abnormalities are
at increased risk for peri-operative events, even if ischaemia cannot
be induced.65
In a meta-analysis of 15 studies comparing dipyridamole thallium-201
imaging and DSE for risk stratification before vascular surgery, it was
demonstrated that the prognostic value of stress imaging abnormalities
for peri-operative ischaemic events is similar with both pharmacological
stressors, but that the accuracy varies with IHD prevalence.61 In patients
with a low prevalence of IHD, the diagnostic accuracy is reduced, compared with those with a high incidence of IHD.
Cardiovascular magnetic resonance (CMR) imaging can be used
for detection of ischaemia; both perfusion and wall motion can be
ESC/ESA Guidelines
Page 13 of 49
ESC/ESA Guidelines
4. Risk-reduction strategies
3.7 Invasive coronary angiography

Coronary angiography is a well-established, invasive, diagnostic
procedure but is rarely indicated for assessing the risk of patients
undergoing non-cardiac surgery. There is a lack of information
from randomized clinical trials, relating to its usefulness in patients
scheduled for non-cardiac surgery. Also, adopting an invasive coronary angiography assessment may cause an unnecessary and unpredictable delay in an already planned surgical intervention, as
well as adding an independent procedural risk to the overall risk.
Despite the fact that CAD may be present in a significant number
of patients requiring non-cardiac surgery, indications for preoperative coronary angiography and revascularization are similar
to angiography indications in the non-surgical setting.56,72 75 Preoperative treatment of myocardial ischaemia, either medically or
with intervention, is recommended whenever non-cardiac
surgery can be delayed.
Class a
Levelb
Ref. c
Indications for pre-operative

coronary angiography and
revascularization are similar
to those for the non-surgical
setting.
56
Urgent angiography is
with acute ST-segment
elevation myocardial
infarction requiring nonurgent, non-cardiac surgery.
75
Urgent or early invasive

strategy is recommended in
patients with NSTE-ACS
requiring non-urgent, noncardiac surgery according to
risk assessment.
73
Pre-operative angiography is
with proven myocardial
ischaemia and unstabilized
chest pain (Canadian
Cardiovascular Society Class
IIIIV) with adequate medical
therapy requiring non-urgent,
non-cardiac surgery.
56,72
Pre-operative angiography
may be considered in stable
cardiac patients undergoing
non-urgent carotid
endarterectomy surgery.
IIb
76
Pre-operative angiography is
not recommended in cardiacstable patients undergoing
low-risk surgery.
III
Recommendations
NSTE-ACS non-ST-segment elevation acute coronary syndromes.

a
b
Level of evidence.
c
The stress of surgery and anaesthesia may trigger ischaemia through

an increase in myocardial oxygen demand, a reduction in myocardial
oxygen supply, or both. Besides specific risk-reduction strategies
adapted to patient characteristics and type of surgery, pre-operative
evaluation can check and optimize the control of cardiovascular risk
factors.
4.1.1 Beta-blockers
Concerns were raised over a number of studies of the Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography (DECREASE) family,77 and the results of these studies were
not included in the present Guidelines.
The main rationale for peri-operative beta-blocker use is to decrease myocardial oxygen consumption by reducing heart rate,
leading to a longer diastolic filling period and decreased myocardial
contractility. Additional cardioprotective factors have been suggested; however, the answer to whether or not this translates into
clinical benefit requires randomized trials analysing the incidence of
cardiovascular events. Six randomized trials evaluating the effect of
peri-operative beta-blockade on clinical endpoints have been published in English in peer-reviewed journals (Table 5).78 83
Two trials targeted patients at high risk for peri-operative complications relating to the type of surgery, the presence of IHD, or risk
factors for peri-operative cardiac complications.79,83 Three other
trials did not require clinical risk factors, except for diabetes in one
case.80 82 The Peri-Operative ISchemic Evaluation (POISE) trial
covered a wide spectrum of risk of peri-operative cardiac complications.78 One trial randomized 200 patients with at least two IHD risk
factors or with known IHD, who were scheduled for non-cardiac
surgery under general anaesthesia, including 40% for major vascular
surgery.83 Atenolol was associated with a significant decrease in
overall mortality at 6 months, which was sustained for up to 2
years; however, seven in-hospital deaths, five in the atenolol group
and two in the placebo group, were not taken into account. The PeriOperative Beta-BLockadE (POBBLE) trial randomized 103 low-risk
patients undergoing elective infrarenal vascular surgery to metoprolol tartrate or placebo,82 resulting in a similar incidence of death,
myocardial infarction or stroke at 30 days (13% and 15%, respectively;
P 0.78). Patients at low cardiac risk and those with a history of myocardial infarction within the past 2 years were excluded. The
Metoprolol after Vascular Surgery (MaVS) trial randomized 497
patients undergoing abdominal or infra-inguinal vascular surgery
to metoprolol succinate or placebo.80 The combined incidence
of death, myocardial infarction, heart failure, arrhythmias, or stroke
at 30 days was similar (10.2% and 12.0%, respectively; P 0.57).
The revised cardiac risk index was 2 in 90% of patients and 1
in 60%.
The Diabetes Post-Operative Mortality and Morbidity (DIPOM)
trial randomized 921 patients with diabetes, age .39 years, and duration of surgery of .1 hour (39% low-risk surgery) to receive metoprolol succinate or placebo.81 The combined incidence of death,
myocardial infarction, unstable angina, or heart failure at 30 days
was again similar (6% and 5%, respectively; P 0.66); however,
only 54% of patients had a history of IHD or an additional cardiac
risk factor, and underwent high- or intermediate-risk surgery.
Recommendations on pre-operative coronary

angiography
4.1 Pharmacological
Page 14 of 49
ESC/ESA Guidelines
Table 5 Summary of randomized, controlled trials evaluating the effect of peri-operative beta-blockade on postoperative mortality and non-fatal myocardial infarction
The POISE trial randomized 8351 patients to metoprolol succinate

or placebo.78 Patients were aged 45 years and had known CVD, or
at least three of seven clinical risk factors for high-risk surgery, or
were scheduled for major vascular surgery. Treatment consisted of
metoprolol succinate 100 mg 24 hours before surgery, 100 mg
during the first 6 hours after surgery, but medication was withheld
if systolic blood pressure dipped below 100 mm Hg. Maintenance
therapy started 12 hours later, bringing the total dose of metoprolol
succinate in the first 24 hours to 400 mg in some patients. There was a
17% decrease in the primary composite endpoint of death, myocardial infarction, or non-fatal cardiac arrest at 30 days (5.8% vs. 6.9%;
P 0.04); however, the 30% decrease in non-fatal myocardial infarction (3.6% vs. 5.1%; P , 0.001) was offset by a 33% increase in total
mortality (3.1% vs. 2.3%; P 0.03) and a doubling of stroke incidence
(1.0% vs. 0.5%; P 0.005). Hypotension was more frequent with
metoprolol (15.0% vs. 9.7%; P , 0.0001). Post-hoc analysis showed
that hypotension carried the greatest attributable risk of death and
stroke.84
Eight meta-analyses have pooled 9, 25, 5, 11, 6, 8, 22, and 33 published, randomized trials on peri-operative beta-blockers, totalling,
respectively, 10 529, 12 928, 586, 866, 632, 2437, 2057, and 12 306
patients.85 92 Four meta-analyses showed a significant reduction in
peri-operative myocardial ischaemia and myocardial infarction in
patients receiving beta-blockers,88,89,91,92 this being more marked

in high-risk patients. Two meta-analyses showed no significant reduction in peri-operative myocardial infarction or cardiac mortality in
patients receiving beta-blockers.87,90 These meta-analyses (except
the two most recent ones)85,86 have been criticized because of heterogeneity of included studies and types of surgery, inclusion of
studies of the DECREASE family, imprecision regarding patients
cardiac risk profiles, and variable timing of beta-blocker administrations, doses, and targets.93 The recent POISE trial had the greatest
weight in all of these analyses. In POISE, all-cause mortality increased
by 33% in patients receiving beta-blockers; peri-operative death
in patients receiving metoprolol succinate were associated with
peri-operative hypotension, bradycardia, and stroke. A history of
cerebrovascular disease was associated with an increased risk of
stroke. Hypotension was related to high-dose metoprolol without
dose titration.
In a meta-analysis that excluded the DECREASE trials,85 perioperative beta-blockade was associated with a statistically significant
27% (95% CI 1 60) increase in mortality (nine trials, 10 529 patients)
but the POISE trial again largely explained this result,78 and also the
reduced incidence of non-fatal myocardial infarction and increased
incidence of non-fatal strokes. Another recent meta-analysis, involving 12 928 patients, examined the influence of beta-blockade on all-
BBSA Beta-Blocker in Spinal Anesthesia; DIPOM Diabetic Postoperative Mortality and Morbidity; IHD ischaemic heart disease; MaVS Metoprolol after Vascular Surgery;
MI myocardial infarction; POBBLE PeriOperative Beta-BlockadE; POISE PeriOperative ISchemic Evaluation.
a
At 6 months and including in-hospital deaths.
b
P 0.0317.
c
P 0.0008.
Page 15 of 49
ESC/ESA Guidelines
atenolol and bisoprolol are superior to metoprolol,97,100 102 possibly

due to the CYP2D6-dependent metabolism of metoprolol. Trials using
metoprolol did not show a clear benefit.78,80 82 A recent single-centre
cohort study in 2462 pair-matched patients suggested that metoprolol
or atenolol (analysed together) are associated with increased risk of
post-operative stroke, compared with bisoprolol.102
Recommendations on beta-blockers
Recommendations
Classa
Levelb
Ref. c
9699
Pre-operative initiation of betablockers may be considered in

patients scheduled for high-risk
surgery and who have 2 clinical
risk factors or ASA status 3.d
IIb
86,95,
97
Pre-operative initiation of betablockers may be considered in

patients who have known IHD or
myocardial ischaemia.d
IIb
83,88,
106
When oral beta-blockade is

initiated in patients who undergo
non-cardiac surgery, the use of
atenolol or bisoprolol as a first
choice may be considered.
IIb
97,100
102
Initiation of peri-operative highdose beta-blockers without

titration is not recommended.
III
78
Pre-operative initiation of betablockers is not recommended in

patients scheduled for low-risk
surgery.
III
86,97
Peri-operative continuation of betablockers is recommended in

patients currently receiving this
medication.
ASA American Society of Anesthesiologists; IHD ischaemic heart disease.

a
b
Level of evidence.
c
d
Treatment should ideally be initiated between 30 days and (at least) 2 days before
surgery, starting at a low dose, and should be continued post-operatively.83,98,103
The target is a resting heart rate 60 70 bpm,86 and systolic blood pressure
.100 mm Hg.79,83
Initiation of treatment and the optimal choice of beta-blocker dose

are closely linked. Bradycardia and hypotension should be avoided. It
is important to prevent overtreatment with fixed, high, initial doses,
and doses should be decreased if this occurs. Beta-blocker dose
should be slowly up-titrated and tailored to appropriate heart rate
and blood pressure targets, requiring that treatment be initiated
ideally more than 1 day (when possible at least 1 week and up to
30 days) before surgery, starting with a low dose.83,98,103 In patients
with normal renal function, atenolol treatment should start with a
50 mg daily dose, then adjusted before surgery to achieve a resting
heart rate of 60-70 bpm86 with systolic blood pressure .100 mm
Hg.83 The heart rate goal applies to the whole peri-operative
period, using intravenous administration when oral administration
is not possible. High doses should be avoided, particularly immediately before surgery. A retrospective study suggests that intra-operative
cause and cardiovascular mortality according to surgery-specific risk

groups, beta-blocker treatment duration, and whether betablockade was titrated to targeted heart rate.86 The benefit of betablockade was found in five high-risk surgery studies and in six
studies using titration to targeted heart rate, of which one and two
trials, respectively, were of the DECREASE family.
Discrepancies in the effects of beta-blockers can be explained by
differences in patient characteristics, type of surgery, and the
methods of beta-blockade (timing of onset, duration, dose titration,
and type of drug). Also, problems arose by the inclusion of trials not
designed to assess the effect on peri-operative cardiac risk or which
used only a single beta-blocker dose before anaesthesia, without
continuation after surgery.87 Two meta-analyses suggested that differences between trials on the cardioprotective effect of betablockers could be attributed to variability in heart rate response.86,94
In particular, the decrease in post-operative myocardial infarction
was highly significant, with tight heart rate control.
In patients with clinical risk factors undergoing high-risk
(mainly vascular) surgery, randomized trials, cohort studies, and
meta-analyses provide some evidence supporting a decrease in
cardiac mortality and myocardial infarction with beta-blockers
(mainly atenolol). Peri-operative beta-blockade is also cost-effective
in these patients; however, patients with myocardial ischaemia as
demonstrated by stress testing are at high risk of peri-operative
cardiac complications despite peri-operative beta-blocker use.
Conversely, in patients without clinical risk factors, randomized trials
and cohort studies suggest that peri-operative beta-blockade does not
decrease the risk of cardiac complications and may even increase this
risk. A possible increase in mortality has been suggested by a retrospective cohort.95 Bradycardia and hypotension may be harmful in
patients with atherosclerosis, and enhance the risk of stroke and
death. Also, peri-operative beta-blocker administration may enhance
post-operative delirium in patients undergoing vascular surgery.
One cannot justify exposing low-risk patients to potential adverse
effects in the absence of proven benefit. The issue remains debatable
in intermediate-risk patients, i.e. those with one or two clinical risk
factors. Increased mortality following pre-operative beta-blocker
withdrawal has been reported in four observational studies.96 99 Betablockers should be continued when prescribed for IHD or arrhythmias. When beta-blockers are prescribed for hypertension, the
absence of evidence for a peri-operative cardioprotective effect with
other antihypertensive drugs does not support a change of therapy.
Beta-blockers should not be withdrawn in patients treated for stable
heart failure due to LV systolic dysfunction. In decompensated heart
failure, beta-blocker therapy should be adjusted to the clinical condition. If possible, non-cardiac surgery should be deferred so it can be
performed under optimal medical therapy in a stable patient. Contraindications to beta-blockers (asthma, severe conduction disorders,
symptomatic bradycardia, and symptomatic hypotension) should be
respected. In patients with intermittent claudication, beta-blockers
have not been shown to worsen symptoms and are therefore not
contra-indicated. In the absence of contra-indications, beta-blocker
dose should be slowly up-titrated, starting at a low dose of a beta1selective agent, to achieve a resting heart rate between 60 and 70
beats per minute (bpm). Beta1-selective blockers without intrinsic
sympathomimetic activity are favoured and evidence exists that
Page 16 of 49
mean arterial pressure should remain above 55 mm Hg.104 Postoperative tachycardia should firstly lead to treatment of the
underlying causefor example, hypovolaemia, pain, blood loss, or
infectionrather than simply increasing the beta-blocker dose.
When beta-blockers are indicated, the optimal duration of perioperative beta-blockade cannot be derived from randomized trials.
The occurrence of delayed cardiac events indicates a need to continue beta-blocker therapy for several months. For patients testing
positive for pre-operative stress, long-term beta-blocker therapy
should be used.
A high priority needs to be given to new, randomized, clinical trials
to better identify which patients derive benefit from beta-blocker
therapy in the peri-operative setting, and to determine the optimal
method of beta-blockade.105
lack of a parenteral formulation; therefore, statins with a long half-life

(e.g. atorvastatin) or extended release formulations (e.g. lovastatin)
may be favoured to bridge the period immediately after surgery
when oral intake is not feasible.
A concern relating to the use of peri-operative statin therapy
has been the risk of statin-induced myopathy and rhabdomyolysis.
Peri-operatively, factors increasing the risk of statin-induced
myopathy are numerous, e.g. the impairment of renal function after
major surgery, and multiple drug use during anaesthesia. Early introduction of statins allows for better detection of potential side-effects.
According to current guidelines, most patients with peripheral
artery disease (PAD) should receive statins. If they have to undergo
open vascular surgery or endovascular intervention, statins should
be continued afterwards. In patients not previously treated, statins
should ideally be initiated at least 2 weeks before intervention
for maximal plaque-stabilizing effects and continued for at least
1 month after surgery. In patients undergoing non-vascular surgery,
there is no evidence to support pre-operative statin treatment if
there is no other indication.
Recommendations on statins
Classa
Levelb
Peri-operative continuation of
statins is recommended,
favouring statins with a long
half-life or extended-release
formulation.
Pre-operative initiation of
statin therapy should be
considered in patients
undergoing vascular surgery,
ideally at least 2 weeks before
surgery.
IIa
Recommendations
Ref.c
112,113,
115
Level of evidence.
c
b
4.1.3 Nitrates
Nitroglycerine is well known for reversing myocardial ischaemia. The
effect of peri-operative intravenous nitroglycerine on peri-operative
ischaemia is a matter of debate and no effect has been demonstrated
on the incidence of myocardial infarction or cardiac death. Also perioperative use of nitroglycerine may pose a significant haemodynamic
risk to patients, since decreased pre-load may lead to tachycardia and
hypotension.
4.1.4 Angiotensin-converting enzyme inhibitors and
angiotensin-receptor blockers
Independently of the blood pressure-lowering effect, angiotensin converting enzyme inhibitors (ACEIs) preserve organ function; however,
data from an observational study suggested that, regardless of the prescription of beta-blockers and statins, ACEIs did not decrease the frequency of 30-day or 1-year death or cardiac complications after
major vascular surgery in high-risk patients (revised cardiac index
3).110 Despite the lack of specific data on angiotensin-receptor
4.1.2 Statins
3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors
(statins) are widely prescribed in patients with orat risk of IHD. Patients
with non-coronary atherosclerosis (carotid, peripheral, aortic, renal)
should receive statin therapy for secondary prevention, irrespective
of non-cardiac surgery. Statins also induce coronary plaque stabilization through pleiotropic effects, which may prevent plaque rupture
and subsequent myocardial infarction in the peri-operative period.
Multiple observational studies have suggested that peri-operative
statin use has a beneficial effect on the 30-day rate of death or myocardial infarction, and on long-term mortality and cardiovascular event
rates.107 110 In a prospective, randomized, controlled trial, 100
patients scheduled for vascular surgery were allocated to 20 mg of
either atorvastatin or placebo once daily for 45 days, irrespective of
their serum cholesterol concentrations.111 At 6-month follow-up,
atorvastatin significantly reduced the incidence of cardiac events (8%
vs. 26%; P 0.03). In patients in whom statins were introduced
before intervention, two meta-analyses showed a significant reduction
in the risk of post-operative myocardial infarction following invasive
procedures,112,113 however, these meta-analyses included more clinical trials relating to cardiac surgery or percutaneous procedures than to
non-cardiac surgery. All-cause post-operative mortality was not
reduced in most series, except in one observational study that used
propensity score adjustment to account for differences in patient characteristics according to the treatment.114 A recent Cochrane review
focusing on vascular surgery in statin-nave patients did not find any significant difference between statin-treated and control groups for the
separate endpoints of all-cause mortality, cardiovascular mortality,
and myocardial infarction, but these endpoints were assessed in only
178 patients.115 Statins have also been associated with a decreased
risk of complications after endovascular repair of AAA and a decreased
risk of stroke after carotid stenting.116,117
Observational series suggest that peri-operative statin therapy is
also associated with a lower risk of acute renal failure and with
lower mortality in patients experiencing post-operative complications or multiple organ dysfunction syndrome.114 Statins may decrease the risk of post-operative atrial fibrillation (AF) following
major non-cardiac surgery.
Statin withdrawal more than four days after aortic surgery is associated with a three-fold higher risk of post-operative myocardial ischaemia.118 A potential limitation of peri-operative statin use is the
ESC/ESA Guidelines
Page 17 of 49
ESC/ESA Guidelines
Recommendations on use of ACEIs and ARBs

Classa
Levelb
Continuation of ACEIs or ARBs,

under close monitoring, should be
considered during non-cardiac surgery
in stable patients with heart failure
and LV systolic dysfunction.
IIa
Initiation of ACEIs or ARBs should be

considered at least 1 week before
surgery in cardiac-stable patients with
heart failure and LV systolic
dysfunction.
IIa
Transient discontinuation of ACEIs or

ARBs before non-cardiac surgery in
hypertensive patients should be
considered.
IIa
Recommendations
ACEI angiotensin converting enzyme inhibitor; ARB angiotensin receptor

blocker; LV left ventricular.
a
b
Level of evidence.
4.1.5 Calcium channel blockers

The effect of calcium channel blockers on the balance between myocardial oxygen supply and demand makes them theoretically suitable
for risk-reduction strategies. It is necessary to distinguish between
dihydropyridines, which do not act directly on heart rate, and diltiazem or verapamil, which lower the heart rate.
The relevance of randomized trials assessing the peri-operative
effect of calcium channel blockers is limited by their small size, lack
of risk stratification, and the absence of systematic reporting of
cardiac death and myocardial infarction. A meta-analysis pooled 11
randomized trials totalling 1007 patients. All patients underwent
non-cardiac surgery under calcium channel blocker treatment.
There was a significant reduction in the number of episodes of myocardial ischaemia and supraventricular tachycardia (SVT) in the
pooled analyses; however, the decrease in mortality and myocardial
infarction reached statistical significance only when both endpoints
were combined in a composite of death and/or myocardial infarction

(relative risk 0.35; 95% CI 0.08 0.83; P , 0.02). Subgroup analyses
favoured diltiazem. Another study in 1000 patients undergoing
acute or elective aortic aneurysm surgery showed that dihydropyridine use was independently associated with an increased incidence of
peri-operative mortality.119 The use of short-acting dihydropyridinesin particular, nifedipine capsulesshould be avoided.
Thus, although heart rate-reducing calcium channel blockers are
not indicated in patients with heart failure and systolic dysfunction,
the continuation or introduction of heart rate-reducing calcium
channel blockers may be considered in patients who do not tolerate
beta-blockers. Additionally, calcium channel blockers should be continued during non-cardiac surgery in patients with vasospastic angina.
4.1.6 Alpha2 receptor agonists
Alpha2 receptor agonists reduce post-ganglionic noradrenaline
output and might therefore reduce the catecholamine surge during
surgery. The European Mivazerol trial randomized 1897 patients
with IHD who underwent intermediate- or high-risk non-cardiac
surgery. Mivazerol did not decrease the incidence of death or myocardial infarction in the whole population; however, there was a reduction of post-operative death or myocardial infarction observed
in a sub-population of 904 patients undergoing vascular surgery.
The international Peri-Operative ISchemic Evaluation 2 (POISE-2)
trial randomized 10 010 patients undergoing non-cardiac surgery
to clonidine or placebo. Clonidine did not reduce the rate of death
or non-fatal myocardial infarction in general, or in patients undergoing vascular surgery (relative risk 1.08; 95% Cl 0.931.26; P 0.29).
On the other hand, clonidine increased the risk of clinically important
hypotension (relative risk 1.32; 95% Cl 1.241.40; P , 0.001) and
non-fatal cardiac arrest (relative risk 3.20; 95% Cl 1.178.73; P
0.02).120 Therefore, alpha2 receptor agonists should not be administered to patients undergoing non-cardiac surgery.
4.1.7 Diuretics
Diuretics are frequently used in patients with hypertension or heart
failure. In general, diuretics for hypertension should be continued to
the day of surgery and resumed orally when possible. If blood pressure reduction is required before oral therapy can be continued,
other antihypertensive agents may be considered. In heart failure,
dosage increase should be considered if symptoms or signs of fluid
retention are present. Dosage reduction should be considered in
patients with hypovolaemia, hypotension, or electrolyte disturbances. In general, diuretic treatmentif necessary to control
heart failureshould be continued to the day of surgery and
resumed orally when possible. In the peri-operative period, volume
status in patients with heart failure should be monitored carefully
and optimized by loop diuretics or fluids.
The possibility of electrolyte disturbance should be considered in
any patient receiving diuretics. Hypokalaemia is reported to occur in
up to 34% of patients undergoing surgery (mostly non-cardiac). It is
well known to significantly increase the risk of ventricular fibrillation
and cardiac arrest in cardiac disease. In a study of 688 patients with
cardiac disease undergoing non-cardiac surgery, hypokalaemia was
independently associated with peri-operative mortality. Importantly,
the use of K+ and Mg++ -sparing aldosterone antagonists reduces the
risk of mortality in severe heart failure. Special attention should be
blockers (ARBs), the following recommendations apply to ACEIs and

ARBs, given their numerous common pharmacological properties.
Additionally, peri-operative use of ACEIs or ARBs carries a risk of
severe hypotension under anaesthesia, in particular following induction and concomitant beta-blocker use. Hypotension is less frequent
when ACEIs are discontinued the day before surgery. Although this
remains debatable, ACEIs withdrawal should be considered 24
hours before surgery when they are prescribed for hypertension.
They should be resumed after surgery as soon as blood volume
and pressure are stable. The risk of hypotension is at least as high
with ARBs as with ACEIs, and the response to vasopressors may
be impaired. In patients with LV systolic dysfunction, who are in a
stable clinical condition, it seems reasonable to continue treatment
with ACEIs under close monitoring during the peri-operative
period. When LV dysfunction is discovered during pre-operative
evaluation in untreated patients in a stable condition, surgery
should if possible be postponed, to allow for diagnosis of the underlying cause and the introduction of ACEIs and beta-blockers.
Page 18 of 49
given to patients taking diuretics and patients prone to developing
arrhythmias. Any electrolyte disturbanceespecially hypokalaemia
and hypomagnesaemiashould be corrected in due time before
surgery. Acute pre-operative repletion in asymptomatic patients
may be associated with more risks than benefits; thus, minor asymptomatic electrolyte disturbances should not delay acute surgery.
4.2 Peri-operative management in

patients on anti-platelet agents
which depends on the peri-operative bleeding risk, weighed against

the risk of thrombotic complications.
4.2.2 Dual anti-platelet therapy
Five to twenty-five percent of patients with coronary stents require
non-cardiac surgery within 5 years following stent implantation. The
prognosis of stent thrombosis appears to be worse than for de novo coronary occlusion, and premature cessation of dual anti-platelet therapy
(DAPT) in patients with recent coronary stent implantation is the most
powerful predictor for stent thrombosis. The consequences of stent
thrombosis will vary according to the site of stent deployment, e.g.
thrombosis of a left main stem stent is, in most cases, fatal.
The management of anti-platelet therapy, in patients who have
undergone recent coronary stent treatment and are scheduled for
non-cardiac surgery, should be discussed between the surgeon and
the cardiologist, so that the balance between the risk of life-threatening
surgical bleeding on anti-platelet therapybest understood by the
surgeonand the risk of life-threatening stent thrombosis off
DAPTbest understood by the cardiologistcan be considered.
The standard duration for DAPT after bare-metal stenting (BMS) is
different to that for drug-eluting stent (DES) treatment .126
To reduce risk of bleeding and transfusion, current Guidelines recommend delaying elective non-cardiac surgery until completion of
the full course of DAPT and, whenever possible, performing surgery
without discontinuation of aspirin.74 Patients who have undergone a
previous percutaneous coronary intervention (PCI) may be at higher
risk of cardiac events during or after subsequent non-cardiac surgery,
particularly in cases of unplanned or urgent surgery following coronary
stenting. While non-cardiac surgery performed early after balloon
angioplasty is not associated with an increased risk of cardiac
events,127 stenting dramatically changes the scenario. Accordingly,
mortality rates of up to 20% were reported in relation to peri-operative
stent thrombosis when surgery was performed within weeks following
coronary stenting and DAPT was discontinued.128 Therefore, elective
surgery should be postponed for a minimum of 4 weeks and ideally for
up to 3 months after BMS implantation. Importantly, whenever possible, aspirin should be continued throughout surgery.129 In 2002,
DES were introduced in Europe and became widely accepted as an efficient tool for reducing in-stent re-stenosis; however, the major drawback of the first-generation DES was the need for prolonged DAPT
(aspirin plus clopidogrel) for 12 months. A higher risk of non-cardiac
surgery early after DES placement has been reported,126 and a
higher risk for major adverse cardiac events has also been shown
during the first weeks after non-cardiac surgery in patients with
implanted stents.126,130 But, for the new-generation (second- and
third-generation) DES, routine extension of DAPT beyond 6 months
is no longer recommended based on currently available data. Observational data from new-generation zotarolimus-eluting and everolimus-eluting stents suggest that even shorter durations of DAPT may
be sufficient,131 and a randomized study showed a similar outcome
in patients treated with 3 and 12 months of DAPT after PCI.132
In patients undergoing myocardial revascularization for high-risk
ACS, DAPT treatment is recommended for 1 year irrespective of
stent type. Overall, in patients undergoing non-cardiac surgery
after recent ACS or stent implantation, the benefits of early
surgery for a specific pathology (e.g. malignant tumours, vascular aneurysm repair) should be balanced against the risk of stent thrombosis and the strategy should be discussed.
4.2.1 Aspirin
Peri-operative evaluation of the impact of aspirin continuation or cessation on serious cardiovascular events or bleeding has disclosed controversial results with, on the one hand, a reduction of intra- and
peri-operative strokebut without influence on myocardial infarction during non-cardiac surgeryand, on the other hand, no statistical
significance for the combined endpoint of vascular events. Additionally, concerns of promoting peri-operative haemorrhagic complications have often led to the discontinuation of aspirin in the
peri-operative period. A large meta-analysis, including 41 studies in
49 590 patients, which compared peri-procedural withdrawal vs.
bleeding risks of aspirin, concluded that the risk of bleeding complications with aspirin therapy was increased by 50%, but that aspirin did
not lead to greater severity of bleeding complications.121 In subjects
at risk ofor with provenIHD, aspirin non-adherence/withdrawal
tripled the risk of major adverse cardiac events.
The POISE-2 trial randomized 10 010 patients undergoing noncardiac surgery to aspirin or placebo.122 The patients were stratified
according to whether they had not been taking aspirin before the
study (initiation stratum, with 5628 patients) or they were already on
an aspirin regimen (continuation stratum, with 4382 patients). In the
POISE-2 trial, aspirin was stopped at least three days (but usually
seven days) before surgery. Patients less than six weeks after placement
of a bare metal coronary stent, or less than one year after placement of
a drug-eluting coronary stent, were excluded from the trial and the
number of stented patients outside these time intervals was too
small to draw firm conclusions asto the riskbenefit ratio. Additionally,
only 23% of the study population had known prior CAD and patients
undergoing carotid endarterecomy surgery were excluded. Patients
started taking aspirin (at a dose of 200 mg) or placebo just before
surgery and continued it daily (at a dose of 100 mg) for 30 days in
the initiation stratum and for 7 days in the continuation stratum, after
which they resumed their regular aspirin regimen. Aspirin did not
reduce the rates of death or non-fatal myocardial infarction at 30
days (7.0% in the aspirin group vs. 7.1% in the placebo group; hazard
ratio 0.99; 95% CI 0.861.15; P 0.92). Major bleeding was more
common in the aspirin group than in the placebo group (4.6% vs.
3.8%, respectively; hazard ratio 1.23; 95% CI 1.011.49; P 0.04).
The primary and secondary outcome results were similar in the two
aspirin strata. The trial results do not support routine use of aspirin
in patients undergoing non-cardiac surgery, but it is uncertain
whether patients with a low peri-operative bleeding risk and a high
risk of thrombo-embolic events could benefit from low-dose aspirin.
Aspirin should be discontinued if the bleeding risk outweighs the potential cardiovascular benefit.121,123 125 For patients undergoing
spinal surgery or certain neurosurgical or ophthalmological operations,
it is recommended that aspirin be discontinued for at least seven days.
In conclusion, the use of low-dose aspirin in patients undergoing
non-cardiac surgery should be based on an individual decision,
ESC/ESA Guidelines
Page 19 of 49
ESC/ESA Guidelines
4.2.3 Reversal of anti-platelet therapy

For patients receiving anti-platelet therapy, who have excessive or
life-threatening peri-operative bleeding, transfusion of platelets is
recommended.
Table 6
4.3 Peri-operative management in

patients on anticoagulants
Anticoagulant therapy is associated with increased risk of bleeding
during non-cardiac surgery. In some patients, this risk will be outweighed by the benefit of anticoagulants and drug therapy should
be maintained or modified, whereas, in patients at low risk of thrombosis, anticoagulation therapy should be stopped to minimize bleeding complications.
4.3.1 Vitamin K antagonists
Patients treated with oral anticoagulant therapy using vitamin K antagonists (VKAs) are subject to an increased risk of peri- and post-procedural
bleeding. If the international normalized ratio (INR) is 1.5, surgery can
be performed safely; however, in anticoagulated patients with a high risk
of thrombo-embolismfor example, patients with:
AF with a CHA2DS2-VASc [Cardiac failure, Hypertension, Age
75 (Doubled), Diabetes, Stroke (Doubled) Vascular disease,
Age 6574 and Sex category (Female)] score of 4] or
mechanical prosthetic heart valves, newly inserted biological prosthetic heart valves, or
mitral valvular repair (within the past 3 months) or
recent venous thrombo-embolism (within 3 months) or
thrombophilia,
discontinuation of VKAs is hazardous and these patients will need bridging therapy with unfractionated heparin (UFH) or therapeutic-dose
LMWH.69,137 In general, there is better evidence for the efficacy
and safety of LMWH, in comparison with UFH, in bridging to
surgery.69,137 LMWH is usually administered subcutaneously and
weight-adjusted for once- or twice-daily administration without laboratory monitoring. In patients with a high thrombo-embolic risk, therapeutic doses of LMWH twice daily are recommended, and
prophylactic once-daily doses in low-risk patients.137 The last dose of
LMWH should be administered no later than 12 hours before the procedure. Further adjustment of dose is necessary in patients with
Pharmacological features of non-vitamin K antagonist oral anticoagulants
b.i.d. bis in diem (twice daily); Cmax maximum concentration; CYP3a4 cytochrome P3a4 enzyme; P gP platelet glycoprotein; q.d. quaque die (once daily).
In summary, it is recommended that DAPT be administered for at

least 1 month after BMS implantation in stable CAD,133 for 6 months
after new-generation DES implantation,133 and for up to 1 year in
patients after ACS, irrespective of revascularization strategy.133 Importantly, a minimum of 1 (BMS) to 3 (new-generation DES)
months of DAPT might be acceptable, independently of the acuteness of coronary disease, in cases when surgery cannot be delayed
for a longer period; however, such surgical procedures should be performed in hospitals where 24/7 catheterization laboratories are available, so as to treat patients immediately in case of peri-operative
atherothrombotic events. Independently of the timeframe between
DES implantation and surgery, single anti-platelet therapy (preferably
with aspirin) should be continued.
In patients needing surgery within a few days, current ESC Guidelines recommend withholding clopidogrel and ticagrelor for five days
and prasugrel for seven days prior to surgery unless there is a high risk
of thrombosis.74 In contrast, other guidelines recommend using
platelet function tests for optimal timing of surgery, as discussed in
a recent publication.134,135 However, the guidelines do not provide
the ideal platelet function assay or a bleeding cut-off, and more research in this area is needed.
For patients with a very high risk of stent thrombosis, bridging
therapy with intravenous, reversible glycoprotein inhibitors, such as
eptifibatide or tirofiban, should be considered. Cangrelor, the new reversible intravenous P2Y12-inhibitor, has been shown to provide effective platelet inhibition but is not yet available.136 The use of
low-molecular-weight heparin (LMWH) for bridging in these patients
should be avoided. Dual anti-platelet therapy should be resumed as
soon as possible after surgery and, if possible, within 48 hours.
Page 20 of 49
4.3.2 Non-vitamin K antagonist oral anticoagulants

In patients treated with the non-VKA direct oral anticoagulants
(NOACs) dabigatran (a direct thrombin inhibitor), rivaroxaban, apixaban, or edoxaban (all direct factor Xa inhibitors), all of which have a
well-defined on and off action, bridging to surgery is in most cases
unnecessary, due to their short biological half-lives (Table 6).138
An exception to this rule is the patient with high thrombo-embolic
risk, whose surgical intervention is delayed for several days. The
overall recommendation is to stop NOACs for 23 times their respective biological half-lives prior to surgery in surgical interventions
with normal bleeding risk, and 45 times the biological half-lives
before surgery in surgical interventions with high bleeding
risk.139,140 New tests for better quantification of activity levels of
the various NOACs are under development. In general, reduced
kidney function or moderate-to-high increased bleeding risk should
lead to earlier cessation of NOACs. If patients are pre-treated with
dabigatran, which has about an 80% renal excretion rate, the individual glomerular filtration rate determines the time of its cessation
prior to surgery.139,141 Kidney function is thus essential for tailoring
dabigatran therapy, and earlier cessation is recommended for all
NOACs if the bleeding risk is increased.
Because of the fast on-effect of NOACs (in comparison with
VKAs), resumption of treatment after surgery should be delayed
for 1 2 (in some cases 35) days, until post-surgical bleeding tendency is diminished.
4.3.3 Reversal of anticoagulant therapy
4.3.3.1 Vitamin K antagonists
In patients who are receiving VKAs and who require reversal of the
anticoagulant effect for an urgent surgical procedure, low-dose
(2.5 5.0 mg) intravenous or oral vitamin K is recommended. The

effect of vitamin K on INR will first be apparent after 612 hours. If
more immediate reversal of the anticoagulant effect of VKAs is
needed, treatment with fresh-frozen plasma or prothrombin
complex concentrate (PCC), is recommended, in addition to
low-dose intravenous or oral vitamin K.
In patients receiving UFH and requiring reversal of the anticoagulant effect for an urgent surgical procedure, cessation of therapy is
sufficient, because coagulation is usually normal four hours after
cessation. When UFH is given subcutaneously, the anticoagulant
effect is more prolonged. For immediate reversal, the antidote
is protamine sulphate. The dose of protamine sulphate can be
calculated by assessment of the amount of heparin received in the
previous two hours. (http://www.medicines.org.uk/emc/medicine/
10807/spc). The dose of protamine sulphate for reversal of a
heparin infusion is 1 U per 1 U of heparin sodium.
In patients who are receiving LMWHs, the anticoagulant effect
may be reversed within eight hours of the last dose because of
the short half-life. If immediate reversal is required, intravenous
Patient on NOAC presenting

with bleeding
Check haemodynamic status,

basic coagulation tests to assess
for an anticoagulation effect
(e.g. aPTT for dabigatran, etc),
renal function, etc.
Minor
Delay next dose or

discontinue treatment
Symptomatic/supportive
treatment
Moderatesevere
Mechanical compression
Fluid replacement
Blood transfusion
Oral charcoal if
recently ingested*
Very severe
Consideration of rFVIIa
or PCC
Charcoal filtration* /
Haemodialysis*
Figure 2 Management of bleeding in patients taking non-vitamin

K antagonist direct oral anticoagulants. From Camm et al. 2012.144
*With dabigatran; aPTT activated partial thromboplastin time;
NOAC non-vitamin K antagonist direct oral anticoagulant;
PCC prothrombin coagulation complex; rFVIIa activated recombinant factor VII.
moderate-to-high kidney function impairment. It is recommended that

VKA treatment be stopped 35 days before surgery (depending on the
type of VKA), with daily INR measurements, until 1.5 is reached, and
that LMWH or UFH therapy be started one day after discontinuation of
VKAor later, as soon as the INR is ,2.0.
In patients with mechanical prosthetic heart valves, the evidence in
favour of intravenous UFH is more solid; thus in some centres these
patients are hospitalized and treated with UFH until four hours
before surgery, and treatment with UFH is resumed after surgery
until the INR is within the therapeutic range.69 On the day of the procedure, the INR should be checked. Consideration should be given to
postponing the procedure if the INR is .1.5. LMWH or UFH is
resumed at the pre-procedural dose 12 days after surgery, depending on the patients haemostatic status, but at least 12 hours after the
procedure. VKAs should be resumed on day 1 or 2 after surgery
depending on adequate haemostasiswith the pre-operative maintenance dose plus a boosting dose of 50% for two consecutive days;
the maintenance dose should be administrated thereafter. LMWH or
UFH should be continued until the INR returns to therapeutic levels.
Furthermore, the type of surgical procedure should be taken into
consideration, as the bleeding risk varies considerably and affects
haemostatic control. Procedures with a high risk of serious bleeding
complications are those where compression cannot be performed. In
these cases, discontinuation of oral anticoagulants and bridging
therapy with LMWH are warranted. In patients undergoing surgery
with a low risk of serious bleeding, such as cataract- or minor skin
surgery, no change in oral anticoagulation therapy is needed;
however, it is wise to keep INR levels in the lower therapeutic range.
ESC/ESA Guidelines
Page 21 of 49
ESC/ESA Guidelines
protamine sulphate can be used, but anti-Xa activity is never completely neutralized (maximum 50%).
4.3.3.2 Non-vitamin K antagonist oral anticoagulants

When severe bleeding complications occur under the influence of
NOACs, symptomatic treatment should be initiated (Figure 2)
because of the lack of specific antidotes (these are currently under
development). Preliminary data have shown a potential benefit for
the use of PCC or activated PCC when bleeding occurs under the
direct factor Xa inhibitor rivaroxaban, and is also applicable to apixaban142 and dabigatran,143 whereas haemodialysis is an effective
method for eliminating dabigatran from the circulation but does
not help when a direct factor Xa inhibitor has been used (Figure 2).
Recommendations on anti-platelet therapy
Class a
Levelb
It is recommended that aspirin

be continued for 4 weeks after
BMS implantation and for 312
months after DES implantation,
unless the risk of life-threatening
surgical bleeding on aspirin is
unacceptably high.
Continuation of aspirin, in
patients previously thus treated,
may be considered in the perioperative period, and should be
based on an individual decision
that depends on the perioperative bleeding risk, weighed
against the risk of thrombotic
complications.
IIb
121,122
Discontinuation of aspirin
therapy, in patients previously
treated with it, should be
considered in those in whom
haemostasis is anticipated to be
difficult to control during
surgery.
IIa
121,122
Continuation of P2Y12 inhibitor

treatment should be considered
for 4 weeks after BMS
implantation and for 312
months after DES implantation,
unless the risk of life-threatening
surgical bleeding on this agent is
unacceptably high.
IIa
In patients treated with P2Y12

inhibitors, who need to undergo
surgery, postponing surgery for
at least 5 days after cessation of
ticagrelor and clopidogreland
for 7 days in the case of
prasugrelif clinically feasible,
should be considered unless the
patient is at high risk of an
ischaemic event.
IIa
BMS bare-metal stent; DES drug-eluting stent.

a
b
Level of evidence.
c
Ref. c
The role of routine, prophylactic, invasive, coronary diagnostic evaluation and revascularization in reducing coronary risk for non-cardiac
surgery remains ill-defined. Indications for pre-operative coronary
angiography and revascularization, in patients with known or suspected IHD who are scheduled for major non-cardiac surgery, are
similar to those in the non-surgical setting.74 Control of myocardial
ischaemia before surgery is recommended whenever non-cardiac
surgery can be safely delayed. There is, however, no indication for
routinely searching for the presence of myocardial (silent) ischaemia
before non-cardiac surgery.
The main reason for pre-operative myocardial revascularization is
the potential prevention of peri-operative myocardial ischaemia that
leads to necrosis or electric/haemodynamic instability at the time of
surgery. Coronary pathology underlying fatal peri-operative myocardial infarctions revealed that two-thirds of the patients had significant
left-main or three-vessel disease.145 Most of the patients did not
exhibit plaque fissuring and only one-third had an intracoronary
thrombus. These findings suggest that a substantial proportion of
fatal peri-operative myocardial infarctions may have resulted from
low-flow, high-demand ischaemia, owing to the stress of the operation in the presence of fixed coronary artery stenoses and therefore
amenable to revascularization. In patients who underwent coronary
angiography before vascular surgery, a number of non-fatal perioperative myocardial infarctions occurred as a consequence of
plaque rupture in arteries without high-grade stenosis. These
results are not surprising, considering the extreme and complex
stress situations associated with surgerysuch as trauma, inflammation, anaesthesia, intubation, pain, hypothermia, bleeding, anaemia,
fasting, and hypercoagulabilitywhich may induce multiple and
complex pathophysiological responses.146
The Coronary Artery Surgery Study (CASS) database includes
almost 25 000 patients with CAD, initially allocated to either coronary artery bypass graft (CABG) surgery or medical management,
with a follow-up of .10 years, and 3368 underwent non-cardiac
surgery during follow-up.147 A retrospective analysis of this population suggested that vascular, abdominal, and major head and
neck surgeries were associated with a higher risk of peri-operative
myocardial infarction and death in the presence of nonrevascularized CAD. Furthermore, the study showed that patients
who were clinically stable in the years after CABG had a reduced risk
of cardiac complications in the event that they required non-cardiac
surgery. This protective effect of previous coronary revascularization was more pronounced in patients with triple-vessel CAD
and/or depressed LV function, as well as in those undergoing highrisk surgery, and lasted for at least six years; however, the study was
performed at a time when medical therapy did not meet current
standards. It can be concluded that asymptomatic patients who
underwent CABG within the previous six years are relatively protected from myocardial infarction complicating non-cardiac
surgery and may undergo non-cardiac surgery without routine preoperative stress testing. This may not be the recommendation for
patients with decreased LV function, as illustrated in a small
cohort of 211 patients who underwent non-cardiac surgery
within one year of CABG and in whom peri-operative predictors
for mortality at one year were: LV ejection fraction (LVEF)
,45% (P , 0.001), elevated right ventricular systolic pressure
Recommendations
4.4 Revascularization
Page 22 of 49
ESC/ESA Guidelines
(P 0.03), emergency operation (OR 6.8), need for dialysis (P

0.02) or ventilator support (P 0.03).148
As mentioned above, patients who have had a previous PCI may be
at higher risk of cardiac events during or after subsequent non-cardiac
surgery, particularly in cases of unplanned or urgent surgery following
coronary stenting. It is therefore preferable, whenever possible, to
postpone elective surgery until 12 months after DES implantation.149
However, recent data have suggested that, beyond six months following newer-generation DES implantationand, for some specific
DES devices, beyond three months of DES implantationthe perioperative cardiac event rates may be acceptable.126,132,150 Independently of the interval between DES implantation and surgery, aspirin
should be continued and, in cardiac-stable/asymptomatic patients
with recent myocardial infarction treated with stenting, the timing
of non-cardiac, non-urgent surgery will in part be dictated by the
type of stent implanted.
Recommendations
Class a
Level b Ref. c
It is recommended that, except for

high-risk patients, asymptomatic
patients who have undergone CABG
in the past 6 years be sent for nonurgent, non-cardiac surgery without
angiographic evaluation.d
147,148
Consideration should be given to

performing non-urgent, non-cardiac
surgery in patients with recent BMS
implantation after a minimum of 4
weeks and ideally 3 months following
the intervention.d
IIa
129
Consideration should be given to

performing non-urgent, non-cardiac
surgery in patients who have had
recent DES implantation no sooner
than 12 months following the
intervention. This delay may be
reduced to 6 months for the newgeneration DES.d
IIa
149,150
In patients who have had recent

balloon angioplasty, surgeons should
consider postponing non-cardiac
surgery until at least 2 weeks after
the intervention.
IIa
127,151
BMS bare-metal stent; CABG coronary artery bypass graft surgery;

DES drug-eluting stent.
a
b
Level of evidence.
c
d
Aspirin to be continued throughout peri-operative period.
4.4.1 Prophylactic revascularization in patients with

asymptomatic or stable ischaemic heart disease
Giving clear recommendations on prophylactic revascularization in
patients with asymptomatic or stable IHD is challenging, as most of
the data are derived from retrospective studies and registries.
Recommendations on the timing of non-cardiac surgery

in cardiac-stable/asymptomatic patients with previous
revascularization
The Coronary Artery Revascularization Prophylaxis (CARP)

trial compared optimal medical therapy with revascularization
(CABG or PCI) in patients with stable IHD before major vascular
surgery.152 Of 5859 patients screened at 18 centres of the United
States Department of Veterans Affairs, 510 patients were enrolled
in a randomized trial. Patients were included, based on increased
risk for peri-operative cardiac complications, as assessed by the consultant cardiologist on the basis of a combination of cardiovascular
risk factors and the detection of ischaemia on non-invasive testing;
28% of the study patients had three or more clinical risk factors
and 49% had two or more variables as defined by the revised
cardiac risk index. There was no difference in either mortality or perioperative myocardial infarction at 2.7 years after commencement of
the trial. The results of the CARP study indicated that systematic
prophylactic revascularization before vascular surgery does not
improve clinical outcomes in stable patients.
A second prospective, randomized trial included 208 patients,
selected on the basis of a revised cardiac risk index, who were
scheduled for major vascular surgery.153 Patients were randomly
allocated to either a selective strategy in which coronary angiography was performed, based on the results of non-invasive tests,
or to a systematic strategy, in which patients routinely underwent
a pre-operative coronary angiography. While the rate of myocardial
revascularization was higher in the systematic strategy group (58.1%
vs. 40.1%), the peri-operative, in-hospital, adverse cardiac event
rate (defined as mortality, non-fatal myocardial infarction, cerebrovascular accident, heart failure, and need for new cardiac revascularization procedures), although higher in the selective strategy group,
was not significantly different from that in the systematic strategy
group (11.7% vs. 4.8%; P 0.1). In contrast, the long-term
outcome (after 58 + 17 months) in terms of survival and freedom
from cardiac events was significantly better in the systematic strategy group.
A recent randomized, prospective, controlled trial, focussing on a
particular homogeneous subset of non-cardiac surgical interventions
(CEA), examined the value of pre-operative coronary angiography
and stenting in 426 patients without history of CAD or cardiac symptoms and with normal cardiac ultrasound and electrocardiography
results. The patients were randomized to pre-operative coronary
angiography andif neededrevascularization, or to no coronary
angiography. The primary combined endpoint was the incidence of
any post-operative myocardial ischaemic events combined with the
incidence of complications of coronary angiography and stenting.
In the angiography group, 68 patients (31%) experienced a significant
coronary artery stenosis; 66 of these patients underwent stenting
(87% with a DES) and two underwent CABG, with no post-operative
events. In the non-angiography group, nine ischaemic events
were observed (4.2%; P 0.01). In this particular group of patients,
the results suggest a short-term benefit of systematic coronary
angiography.76
Covering 3949 patients enrolled in 10 studies between the years
1996 and 2006 (nine observational and the CARP randomized
trial), a meta-analysis that addressed the value of pre-operative coronary revascularization before non-cardiac surgery revealed no significant difference between coronary revascularization and medical
management groups, in terms of post-operative mortality and
Page 23 of 49
ESC/ESA Guidelines
4.4.2 Type of prophylactic revascularization in patients

with stable ischaemic heart disease
Occasionally, patients with stable IHD may require elective surgery,
which may be postponed for several months and up to a year. There
are no solid data to guide a revascularization strategy in such a case.
It seems reasonable to propose a cardiovascular work-up according
to the ESC Guidelines on stable angina pectoris.56 Revascularization
should be considered, in order to improve symptoms and prognosis
in patients with obstructive CAD. All patients considered for revascularization should receive optimal medical treatment. The timing
of revascularization is critical and depends on the clinical presentation: stable vs. ACS. The type of revascularization, CABG vs. PCI,
depends on the extent of CAD and technical feasibility and is discussed in detail in the ESC Guidelines on myocardial revascularization,74 of which a new edition will be published in 2014.
Percutaneous coronary intervention should be performed to
improve symptoms in stable symptomatic patients with single or
multi-vessel disease, in whom intervention is technically appropriate and procedural risk does not outweigh the potential benefit.
The choice between PCI and CABG, often a matter of debate,
will depend on several factors: according to the 5-year results of
the Synergy between Percutaneous Coronary Intervention with
TAXUS and Cardiac Surgery (SYNTAX) trial, CABG should
remain the standard of care for patients with complex lesions
(high or intermediate SYNTAX scores). For patients with lesscomplex disease (low SYNTAX scores) or left-main coronary
disease (low or intermediate SYNTAX scores) PCI is an acceptable
alternative.155 In the presence of minimal symptoms or their
absence, these patients may be treated medically. If PCI is performed before non-cardiac surgery, according to the previous
edition of these Guidelines, BMS is advocated in order not to
delay the surgery; however, if the data from recent trials evaluating
newer DES devices are confirmed, this recommendation may no
longer be valid and certain new-generation DES may be used in
low-risk patients requiring early non-cardiac surgery.132 If noncardiac surgery cannot be postponed, CABG should be favoured
over BMS-based PCI in patients with a higher risk of re-stenosis
(small diameter vessel; long lesions; multiple stents required; left-
main trunk lesions) unless the need for a shorter duration of

DAPT, using new-generation DES devices, is confirmed.
Recommendations for prophylactic revascularization in
stable/asymptomatic patients
Recommendations
Classa Level b Ref. c
Performance of myocardial
revascularization is recommended
according to the applicable
guidelines for management in stable
coronary artery disease.
Late revascularization after

successful non-cardiac surgery
should be considered, in
accordance with ESC Guidelines on
stable coronary artery disease.
Prophylactic myocardial
revascularization before high-risk
surgery may be considered,
depending on the extent of a stressinduced perfusion defect.
IIb
147
Routine prophylactic myocardial

revascularization before low- and
intermediate-risk surgery in patients
with proven IHD is not
recommended.
III
152
56
IHD ischaemic heart disease.

a
b
Level of evidence.
c
4.4.3 Revascularization in patients with non-ST-elevation

acute coronary syndrome
No trial has yet investigated the role of prophylactic revascularization in patients with NSTE-ACS requiring non-cardiac surgery;
therefore, if the clinical condition requiring non-cardiac surgery is
not life-threatening, priority should be given to the management
of NSTE-ACS. In such cases, the 2011 ESC Guidelines on the
management of NSTE-ACS apply.73 With regard to the type of
coronary revascularization employed in patients later requiring
non-cardiac surgery, most undergo PCI. In the rare scenario of
NSTE-ACS linked with the need for subsequent early non-cardiac
surgery, at the time of PCI, preference should be given either to
BMS, in order to avoid delaying surgery beyond 1 and preferably
3 months, or to new-generation DES if data from recent trials
confirm non-inferiority.156,157 In rare cases, balloon angioplasty
alone may be a reasonable strategy if a good acute result is expected,
because aspirinrather than dual anti-platelet therapymay be
sufficient.156
The value of coronary revascularization for NSTE-ACS, in patients
who later require non-cardiac surgery, has been addressed in a retrospective analysis covering 16 478 patients who, between 1999 and
2004, had a myocardial infarction and underwent hip surgery, cholecystectomy, bowel resection, elective AAA repair, or lower extremity amputation in a period of up to three years following the
myocardial infarction. This study showed that patients who were
revascularized before surgery had an approximately 50% lower
rate of re-infarction (5.1% vs. 10.0%; P , 0.001) as well as 30-day
(5.2% vs. 11.3%; P , 0.001) and 1-year mortality (18.3% vs. 35.8%;
myocardial infarction (OR 0.85; 95% CI 0.48 1.50 and OR 0.95;

95% CI 0.44 2.08, respectively).154 There were no long-term
outcome benefits associated with prophylactic coronary revascularization (OR 0.81; 95% CI 0.40 1.63 for long-term mortality
and OR 1.65; 95% CI 0.70 3.86 for late adverse cardiac events);
thus, in asymptomatic patients or those with stable CAD, prophylactic coronary angiographyand, if needed, revascularization
before non-cardiac surgerydoes not confer any beneficial
effects as compared with optimal medical management in terms
of peri-operative mortality, myocardial infarction, long-term mortality, and adverse cardiac events.
Successful performance of a vascular procedure, without prophylactic revascularization, in a stable coronary patient, does
not imply that the patient would not require subsequent revascularization. Despite the lack of extensive scientific data, myocardial revascularization may be recommended in patients presenting with persistent
signs of extensive ischaemia before elective non-cardiac surgery similar
to non-surgical settings recommended by the ESC Guidelines.56
Page 24 of 49
ESC/ESA Guidelines
P , 0.001) compared with those who were not revascularized. This

large sample, representing real-world practice, suggests that patients
with a recent myocardial infarction can benefit from pre-operative
revascularization.158
Recommendations on routine myocardial
revascularization in patients with NSTE-ACS
Recommendations
Levelb
73,75,
133,158
IIa
133
73
151,156
If non-cardiac surgery can

safely be postponed, it is
recommended that patients
should be diagnosed and
treated in line with the
guidelines on NSTE-ACS.
In the unlikely combination of
a life-threatening clinical
condition requiring urgent
non-cardiac surgery and
revascularization for NSTEACS, the expert team should
discuss, case by case, the
priority of surgery.
In patients who have
undergone non-cardiac
surgery, aggressive medical
treatment and myocardial
revascularization according to
the guidelines on NSTE-ACS
are recommended following
surgery.
If PCI is indicated before semiurgent surgery, the use of
new-generation DES, BMS or
even balloon angioplasty is
recommended.
Ref. c
ACS acute coronary syndromes; BMS bare-metal stent; DES drug-eluting

stent; NSTE-ACS non ST-elevation acute coronary syndrome; PCI
percutaneous coronary intervention.
a
b
Level of evidence.
c
5. Specific diseases
Several specific diseases merit special consideration in terms of
cardiovascular pre-operative assessment.
5.1 Chronic heart failure

The diagnosis of heart failure requires the presence of symptoms and
signs typical of heart failure and, in addition, evidence of reduced LV
function [heart failure with reduced LVEF (HF-REF)] or a non-dilated
left ventricle with normal or nearly normal systolic function and relevant structural disease and/or diastolic dysfunction [heart failure with
preserved LVEF (HF-PEF)].159 The prevalence of heart failure in
developed countries is 12%, but rises to 10% among persons
70 years of age.160
Heart failure is a well-recognized factor for peri-operative and
post-operative cardiac events and is an important predictor in
several commonly used risk scores.41 43,161 164 In a large registry
Classa
analysis of 160 000 Medicare procedures on patients aged 65

years, heart failure was present in 18% and was associated with a
63% increased risk of operative mortality and a 51% greater risk of
30-day all-cause re-admission, compared with the CAD group or
patient group without heart failure.163 A reduced LVEF of 35%
was found to be a strong predictor of post-operative cardiac
events following vascular surgery.165 The prognostic impact of
HF-PEF on peri-operative morbidity and mortality is not well
defined. One study found no significant differences in events
between controlled HF-PEF and HF-REF patients undergoing noncardiac surgery,166 whereas another found that only those with severely depressed LVEF (,30%) had increased peri-operative event
rates, compared with a group with moderate (LVEF 30 40%) or
mildly (LVEF .40, ,50%) reduced LV function.167 Compared with
HF-REF patients, HF-PEF patients tend to be older, female, more
likely to have hypertension and AF, and less likely to have CAD; generally,
their prognoses are also better.168 In the absence of evidence-based
studies, the similar peri-operative management can be recommended
in patients with HF-PEF as in patients with HF-REF, with emphasis also
on parameters besides LVEF, such as general clinical status, evidence
of volume overload, and increased levels of natriuretic peptides.
Transthoracic echocardiography (TTE) is a key element in the preoperative assessment of patients with known or suspected heart
failure. LVEF, as well as LV and atrial volumes should be measured
with bi-planar or three-dimensional echocardiography.169 Assessments of valve function and diastolic function (such as E/e ratio)
are likewise of major importance,170 as is evaluation of inferior vena
cava diameter for the determination of volume status and right
atrial pressure. Deformation imaging with strain analysis may reveal
dysfunction that is not apparent using traditional methods.170 The information on cardiac structure and function obtained by TTE provides important prognostic information before non-cardiac
surgery.59,171 Thus, routine pre-operative echocardiography should
be considered in high-risk surgical populations; however, routine
echocardiography is not indicated in every cardiac patient. In a
large Canadian cohort study, pre-operative echocardiography was
not associated with improved survival or shorter hospital stay following major non-cardiac surgery.172 In emergency non-cardiac surgery,
a pre-operative-focussed TTE examination may significantly alter
diagnosis and management.173 In patients with a poor echocardiographic window, CMR imaging is an excellent method for the evaluation of both cardiac structure and function.174
The pre-operative levels of natriuretic peptides (BNP or NT
proBNP) are strongly correlated to the prognosis of heart failure
and to peri-operative and post-operative morbidity and mortality.3,175,176 Compared with a pre-operative natriuretic-peptide measurement alone, additional post-operative natriuretic-peptide
measurement enhanced risk stratification for the composite outcomes of death or non-fatal myocardial infarction at 30 days
and 180 days after non-cardiac surgery.55 Thus, the assessment
of natriuretic peptides should form part of a routine pre-operative
evaluation when cardiac dysfunction is known or suspected.
The best assessment of a patients overall functional capacity is
achieved by performing a cardiopulmonary exercise test (CPX/
CPET).177 Both the cardiac and pulmonary reserve and their interaction can then be evaluated; this is far more accurate than judging
the capacity by interview alone. An anaerobic threshold of
,11 mL O2/kg/min has been used as a marker of increased risk.177
Page 25 of 49
ESC/ESA Guidelines
from the non-surgical setting. The evaluation should include physical

examination, ECG, serial biomarker measurements for both
ischaemic myocardial damage and natriuretic peptides, X-ray, and
echocardiography. Special attention should be given to the patients
volume status since high-volume infusion is often needed in the
intra-operative and immediate post-operative setting. In the period
after surgery, fluids given during the operation may be mobilized,
causing hypervolaemia and pulmonary congestion. Careful attention
to fluid balance is therefore essential.
Once the aetiology of post-operative heart failure has been diagnosed, treatment is similar to the non-surgical setting. Patients who
develop heart failure have a significantly increased risk of hospital readmission after surgical procedures, confirming the need for careful
discharge planning and close follow-up, ideally using a multidisciplinary approach.159
Recommendations on heart failure
Recommendations
Classa
Levelb Ref. c
It is recommended that patients with

established or suspected heart failure,
and who are scheduled for noncardiac intermediate or high-risk
surgery, undergo evaluation of LV
function with transthoracic
echocardiography and/or assessment
of natriuretic peptides, unless they
have recently been assessed for these.
55,165,
167,175,176

established heart failure, who are
scheduled for intermediate or highrisk non-cardiac surgery, be
therapeutically optimized as
necessary, using beta-blockers, ACEIs
or ARBs, and mineralocorticoid
antagonists and diuretics, according to
ESC Guidelines for heart failure
treatment.
159
In patients with newly diagnosed heart

failure, it is recommended that
intermediate- or high-risk surgery be
deferred, preferably for at least 3
months after initiation of heart failure
therapy, to allow time for therapy uptitration and possible improvement of
LV function.
164
It is recommended that beta blockade

be continued in heart failure patients
throughout the peri-operative period,
whereas ACEIs/ARBs may be omitted
on the morning of surgery, taking into
consideration the patients blood
pressure. If ACEIs/ARBs are given, it is
important to carefully monitor the
patient's haemodynamic status and
give appropriate volume replacement
when necessary.
Unless there is adequate time for

dose-titration, initiation of high-dose
beta-blockade before non-cardiac
surgery in patients with heart failure is
not recommended.
III
ACEI angiotensin converting enzyme inhibitor; ARB angiotensin receptor

blocker; ESC European society of cardiology; LV left ventricular.
a
b
Level of evidence.
c
Two review papers have assessed the role of CPX as a pre-operative

evaluation tool.178,179 Meta-analyses are difficult, due to heterogeneity in methodology and outcome measures. There are no blinded
studies and the CPX results may influence the decision on whether
to operate on a patient with a potentially serious disease and prognosis. One of the above papers concludes that paucity of robust data
precludes routine adoption of CPX in risk-stratifying patients undergoing major vascular surgery,178 while the other reports that peak
oxygen consumptionand possibly anaerobic thresholdare
valid predictors of peri-operative morbidity and mortality in patients
undergoing non-cardiopulmonary thoraco-abdominal surgery.179
The current ESC Guidelines on acute and chronic heart failure give a
strong recommendation for the use of optimal tolerated doses of ACE
inhibitors (or ARBs in the case of ACE intolerance), beta-blockers, and
aldosterone antagonists as primary treatment strategies in patients
with HF-REF, to reduce morbidity and mortality.159 Digitalis is a
third-level drug to be considered in patients treated optimally with
recommended drugs.159 All patients with heart failure, who are scheduled for non-cardiac surgery, should be treated optimally according to
these recommendations. Furthermore, HF-REF patients with LVEF
35% and left bundle branch block with QRS 120 ms should be evaluated with respect to cardiac resynchronization therapy (CRT) or
CRT-defibrillator (CRT-D) therapy before major surgery.159 Diuretics
are recommended in heart failure patients who have signs or symptoms of congestion (see section 4.1.7).159
In patients with newly diagnosed severe systolic heart failure, it is
recommended that non-urgent surgery be deferred for at least
three months to allow a new medical therapy and/or intervention
ample time to improve LV function and LV remodelling.164 Rapid preoperative initiation of high doses of beta-blockers78 and/or ACEIs,
without adequate time for dose titration, is not recommended.
Patients with heart failure should preferably be euvolemic before
elective surgery, with stable blood pressure and optimal end-organ
perfusion.
Although continuation of ACEIs/ARBs until the day of surgery has
been associated with an increased incidence of hypotension,180 it is
in general recommended that all heart-failure medications, such as
ACE inhibitors, ARBs, and beta-blockers, be continued and that the
patients haemodynamic status be carefully monitored and give
appropriate volume replacement when necessary. In patients considered susceptible to hypotension, transient discontinuation
the day before surgery may be considered. Evening dosage of
ACEIs/ARBs the day before surgeryand not on the morning of
surgerymay be considered in order to avoid hypotension,
whereas beta-blockade should be continued if possible. Heart
failure medications should be re-instituted post-operatively, as
soon as clinical conditions allow. Consider also the possibility of
giving the medications via nasogastric tube or bioequivalent intravenous dose. Regarding patients with LV-assist devices, who are
scheduled for non-cardiac surgery, they should be evaluated
pre-operatively by the centre responsible for implantation and
follow-up. Patients with HF-PEF have an increased stiffness of the
left ventricle and are susceptible to pulmonary oedema with
fluid overload. Adequate peri-operative monitoring, attention to
volume status, control of afterload, and adequate diuretic treatment
are important considerations for these patients.
Post-operative heart failure may pose diagnostic challenges,
as it often presents atypically and may have a different aetiology
Page 26 of 49
5.2 Arterial hypertension
Recommendations on arterial hypertension
Recommendations
Classa Levelb Ref. c

a new diagnosis of hypertension preoperatively be screened for end-organ
damage and cardiovascular risk
factors.
Large peri-operative fluctuations in

blood pressure in hypertensive
patients should be avoided.
IIa
187
Clinicians may consider not deferring

non-cardiac surgery in patients with
grade 1 or 2 hypertension (systolic
blood pressure <180 mm Hg; diastolic
blood pressure <110 mm Hg).
IIb
182
Level of evidence.
b
c
5.3 Valvular heart disease

Patients with VHD are at increased risk of peri-operative cardiovascular complications during non-cardiac surgery.69 The risk is highly
variable, according to the type and severity of VHD and the type of
5.3.1 Patient evaluation
Echocardiography should be performed on any prospective noncardiac surgery patient with known or suspected VHD, in order to
assess its severity and consequences. This is particularly relevant in
the presence of a cardiac murmur. In the presence of severe VHD,
it is recommended that a clinical and echocardiographic evaluation
be performed and, if necessary, treated before non-cardiac surgery.
As for the general evaluation of a patient with VHD, the key issues
are to assess the severity of VHD, the symptoms and their relationship to VHD, and the estimated risks of valvular intervention and of
cardiac complications according to the type of non-cardiac surgery.
The usual classification of non-cardiac surgery, using the three risk
groups defined in Table 3, should also be used in patients with VHD.
5.3.2 Aortic stenosis
Aortic stenosis is the most common VHD in Europe, particularly
among the elderly. Severe aortic stenosis is defined according to an
integrative approach taking into account valve area (,1.0 cm2 or
0.6 cm2/m2 body surface area, except in obese patients), and flowdependent indices (maximum jet velocity 4 m/sec and mean aortic
pressure gradient 40 mm Hg).
Severe aortic stenosis constitutes a well-established risk factor for
peri-operative mortality and myocardial infarction. In the case of
urgent non-cardiac surgery in patients with severe aortic stenosis,
such procedures should be performed under more invasive haemodynamic monitoring, avoiding rapid changes in volume status and
In general, the presence of arterial hypertension is a risk factor, but

not a very strong independent one for cardiovascular complications
in non-cardiac surgery. In a systematic review and meta-analysis of
30 observational studies, pre-operative hypertension was associated with a 35% increase in cardiovascular complications;181
however, uncontrolled blood pressure is one of the commonest
causes of deferred operation.182 When raised blood pressure is discovered in a pre-operative evaluation, it is advisable to search for
target organ damage and evidence of associated cardiovascular
pathology (ECG, renal function parameters, and evidence of
heart failure), and to initiate therapy to lower the blood pressure
to an appropriate level; this is particularly important for those
with concomitant risk factors. It is also important to validate the
diagnosis by multiple measurements, considering ambulatory monitoring if necessary.183
During the induction of anaesthesia, sympathetic activation can
cause an increase in blood pressure of 2030 mm Hg and a heart
rate increase of 15 20 bpm in normotensive individuals.184 This
response may be more pronounced in patients with untreated
hypertension. As the period of anaesthesia progresses, patients
with pre-existing hypertension are more likely to experience lability
of intra-operative blood pressure, which may lead to myocardial
ischaemia. Avoiding excessive peaks in pressure is important but
the hypertensive patient may also be unstable, and profound
hypotensionespecially when associated with baroreflex-mediated
tachycardiamay be equally detrimental. In a study on hypertensive
and diabetic patients undergoing non-cardiac surgery, a decrease in
blood pressure of .20 mm Hg for .1 hour was found to be a risk
factor for complications.185 It is recommended that peri-operative
blood pressure be kept at 70 100% of baseline, avoiding excessive
tachycardia. Post-surgical elevation of blood pressure is frequently
brought about by anxiety and pain after awakening, and may return
to normal after treating these factors.
Common reasons for delaying surgery in patients with hypertension are poorly controlled blood pressure of grade 3 (systolic
blood pressure 180 mm Hg and/or diastolic blood pressure
110 mm Hg), discovery of end-organ damage that has not previously been evaluated or treated, or suspicion of secondary hypertension
without properly documented aetiology. In patients with grade 1 or 2
hypertension (systolic blood pressure ,180 mm Hg; diastolic blood
pressure ,110 mm Hg) there is no evidence of benefit from delaying
surgery to optimize therapy.182 In such cases, antihypertensive medications should be continued during the peri-operative period. In
patients with grade 3 hypertension, the potential benefits of delaying
surgery to optimize the pharmacological therapy should be weighed
against the risk of delaying the procedure. In a randomized study,
when compared with deferred surgery, immediate blood pressure
reduction with nifedipine was associated with similar complication
rates but a shorter hospital stay.186
There is no clear evidence favouring one mode of antihypertensive
therapy over another in patients undergoing non-cardiac surgery.
Patients with arterial hypertension should be managed according
to existing ESC Guidelines.183 For more information on perioperative use of hypertensive medications, see section 4.1.
ESC/ESA Guidelines
Page 27 of 49
ESC/ESA Guidelines
5.3.3 Mitral stenosis

Non-cardiac surgery can be performed with relatively low levels of
risk in patients with non-significant mitral stenosis (valve area
.1.5 cm2) and in asymptomatic patients with significant mitral stenosis (valve area ,1.5 cm2) and systolic pulmonary artery pressure
,50 mm Hg. Pre-operative surgical correction of mitral stenosis in
these patients is not indicated. Control of heart rate is essential to
avoid tachycardia, which may cause pulmonary oedema. Attentive
control of fluid overload is also important. Development of AF may
cause serious clinical deterioration. With the high risk of embolism,
anticoagulation control is important.69,189 In asymptomatic patients
with significant mitral stenosis and systolic pulmonary artery pressure .50 mm Hg, and in symptomatic patients, the risk related to
the non-cardiac procedure is significantly higher, and these patients
may benefit from percutaneous mitral commissurotomy (or open
surgical repair) particularly before high-risk surgery.69,189
5.3.4 Primary aortic regurgitation and mitral regurgitation
Non-significant aortic regurgitation and mitral regurgitation do not
independently increase the risk of cardiovascular complications
during non-cardiac surgery. In asymptomatic patients with severe
aortic or mitral regurgitation and preserved LV function, non-cardiac
surgery can be performed without additional risk. Symptomatic
patientsand those who are asymptomatic with severely impaired
LVEF (,30%)are at high risk of cardiovascular complications,
and non-cardiac surgery should be performed only if necessary.69
Patients with severe aortic or mitral regurgitation and heart failure
may benefit from optimization of pharmacological therapy to
produce maximal haemodynamic stabilization before undergoing
high-risk surgery (see section 5.1).
5.3.5 Secondary mitral regurgitation
Secondary mitral regurgitation is due to LV remodelling that causes a
distortion of the subvalvular apparatus on a structurally normal valve.
In the case of non-cardiac surgery, these patients should undergo
peri-operative evaluation and management according to the recommendations for LV systolic dysfunction and, if secondary mitral
regurgitation is due to IHD, those for IHD. Because secondary

mitral regurgitation is variable according to loading conditions, particular attention should be paid to the assessment of volume status
and heart rhythm during the peri-operative period.
5.3.6 Patients with prosthetic valve(s)
Patients who have undergone previous surgical correction of VHD and
have a prosthetic valve can undergo non-cardiac surgery without additional risk, provided that there is no evidence of valve or ventricular
dysfunction. In current practice, the main problem is the need for a
modification of the anticoagulation regimen in patients in the perioperative period, with oral anticoagulants being temporarily replaced
by UFH or LMWH at therapeutic doses (see section 4.3).
5.3.7 Prophylaxis of infective endocarditis
Indications for antibiotic prophylaxis are limited to high-risk patients
undergoing dental care; however, non-specific prophylaxis remains
recommended in all patients at intermediate or high risk of infective
endocarditis. This is of particular importance in the field of noncardiac surgery, given the increasing burden of healthcare-related infective endocarditis. Prophylaxis of infective endocarditis is discussed
in detail in specific ESC guidelines.190
Recommendations on VHD
Classa
Levelb
Clinical and
echocardiographic
evaluation is
recommended in all
patients with known or
suspected VHD, who are
scheduled for elective
intermediate or high-risk
Aortic valve replacement

is recommended in
symptomatic patients with
severe aortic stenosis,
who are scheduled for
elective non-cardiac
surgery, provided that
they are not at high risk
of an adverse outcome
from for valvular surgery.
Aortic valve replacement

should be considered in
asymptomatic patients
with severe aortic
stenosis, who are
high-risk non-cardiac
surgery, provided that
they are not at high risk
of an adverse outcome
from for valvular surgery.
IIa
Elective low or
intermediate-risk noncardiac surgery should be
considered in
asymptomatic patients
with severe aortic
stenosis if there has been
no previous intervention
on the aortic valve.
IIa
Recommendations
Ref. c
69
heart rhythm as far as possible. In the case of elective non-cardiac

surgery, the presence of symptoms is essential for decision-making.69
In symptomatic patients, aortic valve replacement should be considered before elective surgery.69 In patients who are not candidates
for valve replacement, due either to high risks associated with serious
comorbidities or refusal to undergo the operation, non-cardiac
surgery should be performed only if is essential. In patients at high
risk or contra-indicated for aortic valve replacement, balloon aortic
valvuloplasty or, preferably, transcatheter aortic valve implantation
(TAVI) may be a reasonable therapeutic option before surgery.69
The choice between balloon aortic valvuloplasty and TAVI should
take into account the impact of non-cardiac disease on life expectancy and the degree of urgency of the non-cardiac surgery.
In asymptomatic patients, non-cardiac surgery of low to intermediate risk can be performed safely;188 If possible, the absence of symptoms should be confirmed by exercise testing. If high-risk surgery is
planned, further clinical assessment is necessary to assess the risk
of aortic valve replacement. In those at high risk for aortic valve replacement, elective surgery under more invasive haemodynamic
monitoring should be performed only if strictly necessary. In the
remaining patients, aortic valve replacement should be considered
as the initial procedure.69
Page 28 of 49
ESC/ESA Guidelines
Levelb
In symptomatic patients
with severe aortic
stenosis who are
non-cardiac surgery, TAVI
or balloon aortic
valvuloplasty should be
considered by the expert
team if they are at high
risk of an adverse
outcome from for valvular
surgery.
IIa
Elective non-cardiac
surgery should be
considered in patients
with severe valvular
regurgitation, who do not
have severe heart failure
or LV dysfunction.
IIa
Percutaneous mitral
commissurotomy should
be considered in patients
with severe mitral
stenosis, who have
symptoms of pulmonary
hypertension and are
intermediate- or high-risk
IIa
Ref. c
LV left ventricular; TAVI transcatheter aortic valve implantation; VHD

valvular heart disease.
a
b
Level of evidence.
c
5.4 Arrhythmias
Cardiac arrhythmias are a significant cause of morbidity and mortality
in the peri-operative period. Although the mechanisms for
arrhythmias in patients with structural heart disease are reasonably
well-defined, the modulating influence of transient physiological
imbalance in patients undergoing surgery is less certain. Before
surgery, patients with a history of arrhythmias should be reviewed
by a cardiologist. Arrhythmias such as AF and ventricular tachycardia
often indicate underlying structural heart disease; therefore the
discovery of such pre-operative arrhythmias should lead to evaluation, including echocardiography, before surgery.*
5.4.1 New-onset ventricular arrhythmias in the
pre-operative period
Ventricular arrhythmias, including ventricular premature beats
(VPBs) and ventricular tachycardia (VT) are particularly common
in high-risk patients. Monomorphic VT may result from myocardial
scarring, and polymorphic VT is a common result of acute myocardial ischaemia. Pre-operative detection of these arrhythmias
should therefore lead to evaluation including methods such as
echocardiography, coronary angiography (with revascularization)
and, in selected cases, invasive electrophysiological study, as
appropriate.
Treatment steps for VPBs include identifying and correcting the reversible causes (e.g. hypoxia, hypokalemia and hypomagnesaemia).
There is no evidence that VPBs or non-sustained VTs alone are associated with a worse prognosis or that suppressive therapy is beneficial.
The American College of Cardiology/American Heart Association/ESC Guidelines for management of patients with ventricular
arrhythmias and the prevention of sudden cardiac death recommend
that, regardless of the cause, sustained monomorphic VT with
haemodynamic compromise must be treated promptly with electric
cardioversion. Intravenous amiodarone can be used for initial treatment of patients with stable sustained monomorphic VT, to
prevent recurrences.191
Immediate defibrillation is required to terminate ventricular
fibrillation and sustained polymorphic VT. Beta-blockers are useful
in patients with recurrent sustained polymorphic VT, especially if ischaemia is suspected or cannot be excluded. Amiodarone is reasonable for patients with recurrent sustained polymorphic VT in the
absence of long QT syndrome.191 Torsades de pointes (TdP) may
occur and the withdrawal of any offending drugs and correction of
electrolyte abnormalities are recommended. Management with magnesium sulphate should be considered for patients with TdP and long
QT syndrome.192 Beta-blockade, combined with temporary pacing,
is suggested in patients with TdP and sinus bradycardia. Isoproterenol
is recommended in patients with recurrent, pause-dependent TdP,
who do not have congenital long QT syndrome.191
If the diagnosis is unclear, wide-QRS tachycardia should be presumed to be VT until proven otherwise. Calcium channel blockers,
such as verapamil and diltiazem, should not be used in patients to terminate wide-QRS-complex tachycardia of unknown origin, especially
in patients with a history of myocardial dysfunction.191
5.4.2 Management of supraventricular arrhythmias and
atrial fibrillation in the pre-operative period
Supraventricular arrhythmias and AF are more common than ventricular arrhythmias in the peri-operative period. The aetiology of
these arrhythmias is multifactorial. Sympathetic activity, as the
primary autonomic mechanism, can be responsible for triggering AF.
While initiating specific drug therapy, possible aggravating factors
such as respiratory failure or electrolyte imbalance should also be
corrected. No medication is recommended to suppress supraventricular premature beats. Vagal manoeuvres may terminate SVT in some
cases; they usually respond well to treatment with adenosine. In cases
with incessant or commonly recurring SVT in the peri-operative
setting, where prophylactic treatment is needed, beta-blockers,
calcium channel blockers, or amiodarone treatment can be used.
In rare cases (and taking into account the urgency and nature of
planned surgery), pre-operative catheter ablation of the arrhythmia
substrate may be considered, e.g. for patients with Wolff-ParkinsonWhite syndrome and pre-excited AF.
The objective inmanagingperi-operative AFisusuallyventricularrate
control. As recommended in the ESC Guidelines for management of
AF, beta-blockers and calcium channel blockers (verapamil, diltiazem)
are the drugs of choice for rate control.144 Amiodarone can be used
asafirst-linedruginpatientswithheartfailure,since digoxinisfrequently
ineffective in high adrenergic states such as surgery. Beta-blockers
have been shown to accelerate the conversion of AF to sinus rhythm
in the intensive care unit (ICU) after non-cardiac surgery.193 Anticoagulation must be based on the individual clinical situation.
Classa
Recommendations
Page 29 of 49
ESC/ESA Guidelines
5.4.3 Peri-operative bradyarrhythmias

Peri-operative bradyarrhythmias usually respond well to shortterm pharmacological therapy; temporary cardiac pacing is
rarely required. Prophylactic pacing before non-cardiac surgery
is not commonly indicated. Pre-operative establishment of temporary or permanent cardiac pacing may be appropriate for
patients with complete heart block or symptomatic asystolic episodes. The indications for temporary pacemakers during the perioperative period are generally the same as those for permanent
pacemakers. Asymptomatic bifascicular block, with or without
first-degree atrioventricular block, is not an indication for temporary pacing; however, the availability of an external pacemaker for
transcutaneous pacing is appropriate.
Recommendations
Classa
Continuation of oral antiarrhythmic drugs before surgery is

recommended.
Anti-arrhythmic drugs are

recommended for patients with
sustained VT, depending on the
patients characteristics.
Anti-arrhythmic drugs are not

recommended for patients with
VPBs.
III
Continuation of oral antiarrhythmic drugs before surgery is

recommended.
Electrical cardioversion when

haemodynamic instability occurs is
recommended.
Vagal manoeuvres and antiarrhythmic therapy for termination

of SVT in haemodynamically stable
patients is recommended.
Recommendations on bradyarrhythmias and

pacemakers
Classa
Levelb
The indications for temporary

pacemakers during the peri-operative
period are generally the same as those
for permanent pacemakers.
It is recommended that the hospital

nominate a person who is responsible for
programming of the implanted arrhythmia
devices before and after surgery.
Patients with ICDs, whose devices have

been pre-operatively deactivated, should
be on continuous cardiac monitor
throughout the period of deactivation.
External defibrillation equipment should
be readily available.
Patients who have asymptomatic

bifascicular or trifascicular block are not
recommended for routine management
with a peri-operative temporary pacing
wire.
III
Recommendations
Levelb
Levelb
SVT supraventricular tachycardia.

a
b
Level of evidence.
Recommendations for ventricular arrhythmias

Recommendations
Classa
Level of evidence.
VT ventricular tachycardia; VPB ventricular premature beats.

a
b
Level of evidence.
5.5 Renal disease

Impaired renal function is associated with a significantly increased risk
of CVD and is an independent risk factor for adverse post-operative
cardiovascular outcomes, including myocardial infarction, stroke, and
progression of heart failure. The development of acute kidney injury
(AKI) after major surgery reduces long-term survival in patients with
normal baseline renal function.195 Risk factors for the development
of post-operative AKI following non-cardiac surgery have been identified and include age .56 years, male sex, active cardiac failure,
5.4.4 Peri-operative management of patients with

pacemaker/implantable cardioverter defibrillator
Patients with a permanent pacemaker can safely undergo surgery if
appopriate precautions are taken.194 The use of unipolar electrocautery represents a significant risk, as the electrical stimulus from
electrocautery may inhibit demand pacemakers, or may reprogram
the pacemaker. These problems can be avoided or minimized by
using bipolar electrocautery, correct positioning the ground plate
for the electrical circuit. Keeping the electrocautery device away
from the pacemaker, giving only brief bursts, and using the lowest
possible amplitude may also decrease the interference. The pacemaker should be set in an asynchronous or non-sensing mode in
patients who are pacemaker-dependent. This is most easily done in
the operating room by placing a magnet on the skin over the pacemaker. Patients whose underlying rhythm is unreliable should have
pacemaker interrogation after surgery, to ensure appropriate programming and sensing-pacing thresholds.
Interference with the function of implantable cardioverter defibrillators (ICD) can also occur during non-cardiac surgery, as a result of
the electrical current generated by electrocautery. The ICD should
be turned off during surgery and switched on in the recovery phase
before discharge to the ward. The defibrillator function of an ICD
can be temporarily deactivated by placing a magnet on the skin
over the ICD. While the device is deactivated, an external defibrillator should be immediately available.
Recommendations on supraventricular arrhythmias
Page 30 of 49
Table 7
ESC/ESA Guidelines
Summary of definitions of acute kidney injury
presence of ascites, hypertension, emergency surgery, intraperitoneal surgery, pre-operative creatinine elevation, and diabetes mellitus.
Patients with 6 of these factors have a 10% incidence of AKI, and a
hazard ratio of 46 as compared with those with ,3 risk factors.196
Further, the relationship between chronic kidney disease (CKD)
and cardiovascular morbidity/mortality is independent of hypertension and diabetes.
Chronic kidney disease is defined as impaired kidney function or
raised proteinuria, confirmed on two or more occasions at least
three months apart. Here, the estimated glomerular filtration rate
(eGFR) should be calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula, which uses sex, age,
ethnic origin, and serum creatinine concentration. Additionally, proteinuria should be assessed using the urinary albumincreatinine
ratio. Chronic kidney disease is thus classified into six stages of
eGFR and three stages of proteinuria.197 A comparison of the most
recent definitions of AKI is shown in Table 7.
Renal function can be calculated routinely using the CockcroftGault formula, or an eGFR calculated from serum creatinine using
the Modification of Diet in Renal Disease (MDRD) study or the
CKD-EPI equations. The use of newer biomarkers in the diagnosis of
AKI is still under investigation. Normal GFR values are 100130 mL/
min/1.73 m2 in young men, and 90120 mL/min/1.73 m2 in young
women, and vary depending on age, sex, and body size. A cut-off
GFR value of ,60 mL/min/1.73 m2 correlates significantly with
major cardiovascular adverse events. Identification of patients at risk
of peri-operative worsening of renal function is important, in order
to initiate supportive measures such as maintenance of adequate intravascular volume for renal perfusion and use of vasopressors.198
Susceptibility to developing AKI after exposure to a specific
insult has been identified according to a number of observational
studies.199 The most frequent causes for AKI in hospitalized

cardiac patients relate to the combination of a low cardiac
output/high venous pressure, and/or the administration of iodinated contrast media during diagnostic and interventional vascular procedures. Contrast-induced AKI (CI-AKI) is defined as a
rise of serum creatinine of 44 mmol/L (0.5 mg/dL) or a 25% relative rise from baseline at 48 hours (or 5 10% at 12 hours) following contrast administration. It occurs in up to 15% of
patients with chronic renal dysfunction who are undergoing
radiographic procedures.200 Although most cases of CI-AKI are
self-limiting, with renal function returning to normal within 7
days of the procedure, these patients occasionally (in 0.5 12%
of cases) develop overt renal failure, associated with increased
morbidity and mortality. In some, severe renal impairment
necessitates renal-replacement therapy and can lead to permanent renal injury. The pathogenesis of CI-AKI is multifactorial, and
is thought to include a decrease in glomerular filtration and renal
hypoperfusion, together with renal medullary ischaemia, direct
tubular toxicity via reactive oxygen species, and direct cellular
toxicity from the contrast agent.
A number of risk factor scoring systems exist for predicting CI-AKI.
These include the urgency of the procedure, baseline renal function,
diabetes, and contrast volume. A range of strategies has been proposed to prevent CI-AKI, including minimizing the volume of contrast
medium administered, use of less-nephrotoxic contrast agents, provision of prophylactic renal-replacement therapy, patient hydration,
and use of pharmacological agents to counteract the nephrotoxicity
of contrast agents.198
The relationship between the volume of contrast agent administered and the development of CI-AKI is well known, and
exceeding the maximum contrast dose (contrast volume/eGFR) is
AKI acute kidney injury; AKIN Acute Kidney Injury Network; ESRD end-stage renal disease; GFR glomerular filtration rate; KDIGO Kidney Disease: Improving Global
Outcomes; RIFLE Risk, Injury, Failure, Loss, End-stage renal disease; RRT renal replacement therapy.
Page 31 of 49
ESC/ESA Guidelines
strongly associated with the development of CI-AKI. The impact of

the osmolality of contrast agent on nephrotoxicity has been
evaluated in a number of randomized controlled trials, with dissimilar
results; however, based on a number of meta-analyses, the use of low
osmolar contrast media (LOCM) or iso-osmolar contrast media
(IOCM) is recommended in patients with mild, moderate, or
severe CKD, who are undergoing contrast-enhanced radiography.
Numerous studies have addressed the use of renal-replacement
therapies to prevent CI-AKI.201 Although renal-replacement
therapy has a favourable effect, in terms of reducing CI-AKI (relative
risk 0.19; P , 0.001) in patients with stage 4 or 5 CKD, haemodialysis
has been found to be non-beneficial (and potentially harmful) for the
prevention of CI-AKI in those with baseline CKD stage 3.
Recommendations on renal function
Classa
Levelb
Ref. c
Patients undergoing contrast-enhanced radiographic

procedures
Patients should be assessed

for risk of CI-AKI.
IIa
5.6 Cerebrovascular disease
Prevention of contrast-induced nephropathy in

patients with moderate or moderate-to-severe CKD
Hydration with normal

saline is recommended
before administration of
contrast medium.
198
Use of LOCM or IOMC is

recommended.
198
It is recommended that the

volume of contrast media
be minimized.
198
Hydration with sodium

bicarbonate should be
considered before
administration of contrast
medium.
IIa
202
Short-term high-dose
statin therapy should be
considered.
IIa
203
In patients with stage 4 or

5 CKD, prophylactic
haemofiltration may be
considered before complex
intervention or high-risk
surgery.
IIb
201
In patients with stage 3

CKD, prophylactic
haemodialysis is not
recommended.
III
201
Patients with severe CKD
CI-AKI contrast-induced acute kidney injury; CKD chronic kidney disease;

GFR glomerular filtration rate; IOMC iso-osmolar contrast medium;
LOCM low-osmolar contrast medium.
a
b
Level of evidence.
c
The majority of the literature on peri-operative stroke focuses on

cardiac surgery, with an event rate ranging from 2 10%, according
to the type of operation.204 With respect to non-cardiac surgery,
peri-operative stroke has been reported in 0.08 0.7% of patients
undergoing general surgery, in 0.2 0.9% of patients requiring
orthopaedic surgery, in 0.6 0.9% of lung operations, and in 0.8
3.0% of surgeries involving the peripheral vasculature.204,205 The
associated mortality ranges from 18 26%.204,205 A more recent
analysis on 523 059 patients undergoing non-cardiac surgery
reported a lower incidence of peri-operative stroke (0.1%).206
The occurrence of this adverse event was associated with a
700% increase in peri-operative mortality, corresponding to an absolute risk increase exceeding 20%. Multivariate analysis identified
age, history of myocardial infarction within 6 months prior to
surgery, acute renal failure, history of stroke, history of TIA, dialysis,
hypertension, chronic obstructive pulmonary disease (COPD),
and current tobacco use as independent predictors of perioperative stroke, while high body mass index was found to be
protective.206
Peri-operative strokes are mainly ischaemic and cardioembolic
and AF is often the underlying leading condition. Triggers include
the withdrawal of anticoagulation and the hypercoagulable state
related to surgery. Additional aetiologies include atheroembolism, originating from the aorta or the supra-aortic vessels, and
local atherothrombosis in the presence of intracranial smallvessel disease. Hypoperfusionrelated to peri-operative arterial
hypotension and/or severe stenosis of the cervicocranial
vesselsis an unusual cause of peri-operative stroke.207 Rarely,
peri-operative stroke may be due to air, fat, or paradoxical
embolisms.
In an attempt to attenuate the risk of peri-operative stroke, antiplatelet/anticoagulant treatments should be continued whenever
possible throughout the peri-operative period. Alternatively, the
period of drug withdrawal should be kept as short as possible while
weighting thrombo-embolic and haemorrhagic risks (see sections
4.2 and 4.3). Adequate selection of the anaesthetic technique
Recommendations
Pre-procedural hydration with intravenous isotonic fluids is the

most effective method of reducing the risk of CI-AKI.198 Normal
saline or isotonic sodium bicarbonate (1.26%) may be used and peripherally administered, with the advantage that it requires only one
hour of pre-treatment and may therefore present the preferred
option in patients scheduled for urgent or outpatient procedures.202 N-acetyl cysteine may be considered for prophylaxis of
CI-AKI, given its low cost and toxicity profile; however, the evidence for its benefit remains inconclusive. A number of small
studies undertaking alkalinization of urine using a range of agents
(bicarbonate, sodium/potassium citrate, acetazolamide) have
shown a reduction in the incidence of contrast-induced nephropathy; recent information suggesting the use of high-dose statins in
preventing CI-AKI is promising.203 Although there are theoretical
benefits from the use of loop diuretics in early or established AKI,
these have not been supported by data in studies, and diuretics
are therefore not recommended for the prevention or treatment
of AKI.198
Page 32 of 49
Recommendations on patients with suspected or

established carotid artery disease
Recommendations
Classa
Pre-operative carotid artery and

cerebral imaging are recommended in
patients with a history of TIA or stroke
in the preceding 6 months.
Levelb
Pre-operative, routine carotid artery

imaging may be considered in patients
undergoing vascular surgery.
IIb
Whenever possible, continuation of

anti-platelet and statin therapies should
be considered throughout the perioperative phase in patients with carotid
artery disease.
IIa
For patients with carotid artery disease

undergoing non-cardiac surgery, the
same indications for carotid
revascularization should apply as for
the general population.
IIa
Pre-operative routine carotid artery

imaging is not recommended in
patients undergoing non-vascular
surgery.
III
TIA transient ischaemic attack.

a
b
Level of evidence.
5.7 Peripheral artery disease

Patients with PAD (defined as an anklebrachial ratio of ,0.9, or
previously revascularized with surgery or percutaneous transluminal
angioplasty) usually have advanced atherosclerotic disease affecting
most vascular beds in varying degrees and have a worse prognosis
than patients without PAD.210,211 Even in patients without known
CAD, peripheral artery surgery is associated with an increased incidence of peri-operative acute myocardial infarction.212 Peripheral
artery disease is thus an established risk factor for non-cardiac
surgery and it is reasonable to assess the presence of IHD from the
patients history and routine clinical examinations and tests;
however, it is not recommended to routinely perform exercise or
imaging test to detect cardiac ischaemia in PAD patients without clinical symptoms, unless the patient has more than two of the clinical risk
factors detailed in Table 4. In a randomized trial, prophylactic coronary revascularization before major vascular surgery in stable PAD
patients did not reduce the incidence of major clinical endpoints.152
However, patients with severely reduced LV function or left main
disease were excluded.
All patients with PAD should be treated with statins and platelet
inhibitors according to guidelines.211 Blood pressure control and lifestyle measures should be attended to, as recommended in the ESC
Guidelines on cardiovascular prevention.210 It is not recommended
that beta-blocker therapy be routinely initiated pre-operatively
unless there are other indications, such as heart failure or ischaemic
coronary disease (see section 4.1).
(regional vs. neuraxial vs. general anaesthesia), prevention and treatment of AF, euglycaemic control (avoiding both hyperglycaemia and
hypoglycaemia), as well as meticulous peri-operative blood pressure
control, may all contribute to reducing the risk of peri-operative
stroke.
Patients undergoing non-cardiac surgery should be questioned
about previous neurological symptoms, and those with symptoms
suggestive of TIA or stroke in the preceding 6 months should
undergo pre-operative neurological consultation as well as neurovascular and brain imaging, where appropriate. In the absence of
dedicated studies addressing this issue, the criteria for carotid
revascularization described in the 2011 ESC Guidelines on the
diagnosis and treatment of peripheral artery disease should also
guide the management of patients with carotid disease, who are
undergoing non-cardiac surgery.19 In patients with symptomatic
carotid disease (i.e. with a stroke or TIA affecting the corresponding vascular territory in the preceding 6 months), carotid revascularization should performed first and non-cardiac surgery
postponed.
Owing to the increasing average age of the population, an increasing number of patients referred for non-cardiac surgery
may have associated asymptomatic carotid artery disease.
According to a meta-analysis of studies covering a total of 4573
patients with PAD, the rates of asymptomatic carotid stenosis
.50% and .70% were 25% and 14%, respectively.208 Carotid
imaging, while not indicated routinely in patients undergoing noncardiac surgery, may be considered before vascular surgery, due
to the high prevalence of carotid artery disease in this patient
group.
The question as to whether patients with severe asymptomatic
carotid occlusive disease, who are undergoing elective major noncardiac surgery, require pre-operative carotid revascularization
remains a matter of debate. Importantly, the purpose of carotid
revascularization in this setting is more the long-term prevention
of stroke than peri-operative stroke reduction; therefore, if
carotid revascularization is indicated, this may be performed
before or after the planned non-cardiac surgery. Independently of
the revascularization strategy, patients with carotid artery stenosis
benefit from aggressive cardiovascular risk-factor modification to
prevent peri-operative myocardial ischaemia. Accordingly, patients
with carotid artery disease suffer a high incidence of CAD. In a prospective investigation in 390 patients undergoing elective carotid
artery revascularization, systematic coronary angiography showed
the presence of one-, two-, and three-vessel disease, and left main
coronary stenoses in 17%, 15%, 22%, and 7% of patients, respectively.209 Consequently, statins should be continued; whenever possible aspirin and beta-blockers should not be withdrawn, and
blood pressure should be carefully controlled (see sections 4.1
and 5.2).
Apart from TIA or stroke, transient or even permanent changes in
mental status may occur following non-cardiac surgery, including
spatio-temporal disorientation, memory loss, hallucinations,
anxiety or depression. These findings may especially be encountered
in patients with known cognitive impairment. The underlying
mechanisms, often elusive, may include surgery-induced systemic inflammation and cerebral hypoperfusion.
ESC/ESA Guidelines
Page 33 of 49
ESC/ESA Guidelines
Recommendation on PAD
Recommendation
Patients with PAD should be clinically
assessed for ischaemic heart disease and, if
more than two clinical risk factors (Table 4)
are present, they should be considered for
pre-operative stress or imaging testing.
Classa Levelb
IIa
PAD peripheral artery disease.

a
b
Level of evidence.
5.8 Pulmonary disease
The co-existence of pulmonary disease in patients undergoing noncardiac surgery may increase the operative risk. Such diseases
include acute respiratory infections, COPD, asthma, cystic fibrosis,
interstitial lung disease, and other conditions causing impairment of
respiratory function. Pre-existing pulmonary disease has a significant
impact on peri-operative risk, but the most common effect is to increase the risk of post-operative pulmonary complications. These
complications are in part a consequence of the development of atelectasis during general anaesthesia; however, factors that result in
post-operative hypoventilation, reduced tidal volumes, and impaired
lung expansion may cause persistent lung collapse and increase the
risk of respiratory infection. These complications occur particularly
after abdominal or thoracic surgery, and the risk seems to be
increased in smokers. Certain respiratory conditions are associated
with cardiovascular pathology and may require special cardiac risk assessment and management, in addition to dealing with pulmonary
disease per se. Three such conditions are COPD, obesity hypoventilation syndrome (OHS), and pulmonary artery hypertension (PAH).
COPD is characterized by airflow obstruction that is usually progressive, not fully reversible, and does not change markedly over
several months. The disease is predominantly caused by smoking
and is well-recognized as a major cause of morbidity and mortality.213
The prevalence of COPD in Europe is 410% of adults, therefore up
to one patient in ten undergoing non-cardiac surgery may have
COPD. Cor pulmonale with associated right-heart failure may be a
direct complication of severe COPD; however, COPD is also associated with an increased risk of CAD. COPD is a risk factor for
IHD and sudden death by unknown mechanisms, although there
are several shared risk factors for both types of disease (smoking, diabetes, hypertension, systemic inflammation, increased plasma fibrinogen). Epidemiological evidence suggests that reduced forced
expiratory volume in 1 second (FEV1) is a marker for cardiovascular
mortality, independent of age, gender, and smoking history, with a
30% increase in cardiovascular mortality and 20% increase in nonfatal coronary events for every 10% decrease in FEV1.213 Although
patients with COPD have an increased risk of CVD, there is no evidence that COPD is related to a higher risk of peri-operative
cardiac complications. Post-operative pulmonary complications
result in significant mortality and morbidity, however. Pre-operative
evaluation, using specific post-operative pulmonary complication
tools, can be used to stratify patients at risk and allow optimal preoperative and peri-operative management.214
In patients with COPD who are having non-cardiac surgery, the

pre-operative treatment goals are to optimize pulmonary function
and minimize post-operative respiratory complications; this includes
using the pre-operative period for education, including possible cessation of smoking (.2 months before surgery), instruction in chest
physiotherapy and lung expansion manoeuvres, muscular endurance
training, and re-nutrition if required. Beta-adrenergic agonists and
anticholinergic agents should be continued until the day of surgery
in all symptomatic COPD patients with bronchial hyper-reactivity.
In some cases, short-term systemic/inhaled steroids may be considered. Any associated ventricular failure should be managed accordingly. Where there is active pulmonary infection, appropriate
antibiotics should be administered for at least 10 days and, if possible,
surgery should be delayed.215
OHS is defined as the triad of obesity, daytime hypoventilation, and
sleep-disordered breathing. Although distinct from simple obesity and
sleep apnoea, it is estimated that 90% patients with OHS also have obstructive sleep apnoea. The prevalence of OHS is 0.153% of adults,
and 722% in patients undergoing bariatric surgery.216 Obesity and obstructive sleep apnoea are associated with a number of comorbidities
including CAD, heart failure, stroke, and metabolic syndrome. OHS is
associated with even higher morbidity, including heart failure (and
obesity-related cardiomyopathy), angina pectoris, pulmonary hypertension (3088%) and cor pulmonale, and increased peri-operative mortality.216 Pre-operatively, the presence of a high body mass index and
apnoeahypopnea index should alert the physician to screen for
OHS, including the use of screening questionnaires, peripheral
oxygen saturations, and serum bicarbonate levels. Patients at high risk
of OHS who are undergoing major surgery should be referred for additional specialist investigation for sleep disordered breathing and pulmonary hypertension, with pre-operative initiation of appropriate
positive airway pressure therapy, and planning of peri-operative techniques (anaesthetic and surgical) and post-operative positive airway pressure management within an appropriate monitored environment.216
Pulmonary hypertension is a haemodynamic and pathophysiological condition, defined as an increase in mean pulmonary arterial
pressure .25 mm Hg at rest, as assessed by right heart catheterization, and can be found in multiple clinical conditions.217 Pulmonary
artery hypertension (PAH) is a clinical condition, characterized by
the presence of pre-capillary pulmonary hypertension in the
absence of other causes, such as pulmonary hypertension due to
lung diseases, chronic thrombo-embolic pulmonary hypertension,
or other rare diseases. Pulmonary artery hypertension includes different forms that share a similar clinical picture and virtually identical
pathological changes of the lung microcirculation.217 From surveys
and population studies, the prevalence of PAH is reported to be
between 15 150 cases per million adults, with approximately 50%
of cases being idiopathic. The prevalence is thus low and consequently the condition is uncommon in surgical practice. Pulmonary artery
hypertension is associated with increased post-operative complications, including right ventricular failure, myocardial ischaemia, and
post-operative hypoxia and, in patients undergoing cardiopulmonary
bypass surgery, a mean pre-operative pulmonary artery pressure
.30 mm Hg is an independent predictor of mortality. In patients
with pulmonary hypertension undergoing non-cardiac surgery,
outcome predictors include New York Heart Association functional
Class .III, intermediate to high-risk surgery, right ventricular
Page 34 of 49
ESC/ESA Guidelines
dysfunction, and long duration of anaesthesia. This condition has an

associated peri-operative cardiopulmonary complication rate of
38%, and mortality of 7%.218,219 The initial approach after diagnosing
PAH is the adoption of general measures and supportive therapy, and
referral to an expert centre for initiation of advanced pulmonary
hypertensive therapies. Owing to the potential for anaesthesia and
surgery to be complicated by acute right heart failure and pulmonary
hypertensive crisis, surgical interventions in patients with PAH should
be avoided unless absolutely necessary. Ideally, patients with PAH
Recommendations on PAH and pulmonary diseases
Recommendations

PAH have an optimized treatment
regimen before any non-emergency
surgical intervention.
It is recommended that patients
receiving PAH-specific treatment
continue this in the pre-, peri-, and
post-operative period without
interruption.
It is recommended that monitoring
of patients with PAH continue for at
least 24 hours in the post-operative
period.
In the case of progression of right
heart failure in the post-operative
period of patients with PAH, it is
recommended that the diuretic dose
be optimized and, if necessary,
intravenous vasoactive drugs be
initiated under the guidance of a
physician experienced in the
management of PAH.
In patients with COPD, smoking
cessation (>2 months before surgery)
is recommended before undertaking
surgery.
In the case of severe right heart
failure that is not responsive to
supportive therapy, the temporary
administration of pulmonary
vasodilators (inhaled and/or
intravenous) is recommended, under
the guidance of a physician
experienced in PAH.
In patients at high risk of OHS
additional specialist investigation
before major elective surgery should
be considered.
217
217,
220
5.9 Congenital heart disease

I
217
217
217,
221
Children, adolescents and adults with congenital heart disease are

generally regarded as being at increased risk when undergoing noncardiac surgery but this risk will vary enormously, according to the
degree of associated heart failure, pulmonary hypertension, arrhythmias, and shunting of bloodwith or without associated oxygen desaturation and by the complexity of the underlying condition.222 A
thorough understanding of the underlying congenital heart disease,
including anatomy, physiology, and identification of risk factors, is
vital before surgery. When the defect is simple, the circulation physiologically normal and the patient well compensated, the risk may be quite
low; however, complicated patients with congenital heart disease
should only undergo non-cardiac surgery after thorough evaluation
by a multidisciplinary team in a specialized centre. Prophylaxis for endocarditis should be initiated according to the ESC Guidelines on congenital heart disease and infective endocarditis.190,222
Recommendation on patients with congenital heart
disease
Recommendation
It is recommended that, patients with
complex congenital heart disease be
referred for additional specialist
investigation before undergoing elective
non-cardiac surgery, if feasible.
217
Classa
Levelb
Level of evidence.
IIa
216
PAH pulmonary artery hypertension; OHS obesity hypoventilation syndrome.

a
b
Level of evidence.
c
6. Peri-operative monitoring
6.1 Electrocardiography
Continuous ECG monitoring is recommended for all patients undergoing anaesthesia. The patient should be connected to the ECG

severe PAH, who are undergoing
elective surgery, be managed in a
centre with appropriate expertise.
It is recommended that interventions
for high-risk patients with PAH be
planned by the multidisciplinary
pulmonary hypertension team.
who are undergoing surgery should have an optimized treatment

regimen before any surgical intervention, and be managed in a
centre with appropriate expertise. Interventions for high-risk
patients should be planned by the multidisciplinary pulmonary hypertension team. Patients receiving PAH-specific therapy must not have
drugs withheld for the pre-operative fasting state, and may require
temporary conversion to intravenous and/or nebulized treatment
until they are able to reliably absorb via the enteral route. As the
highest mortality is in the post-operative period, it is recommended
that facilities for appropriate monitoring should be available, and
monitoring continued for at least 24 hours. In case of progression
of right heart failure in the post-operative period, it is recommended
that the diuretic dose should be optimized and, if necessary, inotropic
support with dobutamine be initiated. Starting new, specific PAH
drug therapy in the peri-operative period has not been established.
In the case of severe right heart failure that is not responsive to supportive therapy, the temporary administration of pulmonary vasodilators (inhaled and/or intravenous) may be considered, under the
guidance of a physician experienced in PAH.
Page 35 of 49
ESC/ESA Guidelines
Recommendations on ECG monitoring

Recommendations
Peri-operative ECG monitoring is
recommended for all patients
undergoing surgery.
Classa
Levelb Ref. c
Selected lead combinations should be

considered for better detection
of ischaemia in the operating room.
IIa
225,
226
When feasible, twelve-lead ECG

monitoring should be considered
for high-risk patients undergoing
surgery.
IIa
227,
228
ECG electrocardiogram.
a
b
Level of evidence.
c
6.2 Transoesophageal echocardiography

Transoesophageal echocardiography (TOE) has frequently been
used as a monitoring tool during cardiac surgery. TOE has
several advantages. It is rapidly available, relatively non-invasive,
and provides more versatile and comprehensive information;
however, although TOE is in general a safe procedure, serious
adverse events can occur. The complication rates relate to the experience of the operator and the presence of oesophageal or
gastric diseases. Specific training of users is essential to avoid inaccurate interpretation.
Myocardial ischaemia can be identified by abnormalities in regional wall motion and thickening. The agreement between
intra-operative TOE and ECG is rather weak.229 Both ST-segment
changes and regional wall motion abnormalities can be present in
the absence of acute ischaemia. Wall motion abnormalities may
be difficult to interpret in the presence of left bundle branch
block, ventricular pacing, or right ventricular overload. The resolution of ischaemia is not necessarily detectable if ischaemia is followed by myocardial stunning. Episodes of new or worsened wall
motion abnormalities have been shown to be relatively infrequent
(20%) in high-risk patients undergoing non-cardiac surgery.229
They were more common in patients submitted to aortic vascular
surgery. Episodes were poorly correlated with post-operative
cardiac complications.229
For the purpose of identifying patients at high risk of peri-operative
ischaemic outcomes, routine monitoring for myocardial ischaemia with
TOE or 12-lead ECG during non-cardiac surgery is of little more clinical
value than pre-operative clinical data and intra-operative monitoring
using a 12-lead ECG.230
TOE is recommended if acute and severe haemodynamic
instability or life-threatening abnormalities develop during or after
surgery.231 It is a useful technique in the context of hypotension
during non-cardiac surgery. In a prospective study including 42
adults, TOE was performed before any other haemodynamic monitoring when severe hypotension developed. It was useful for determining the cause of severe hypotension, hypovolaemia, low
ejection fraction, severe embolism, myocardial ischaemia, cardiac
tamponade, or dynamic LV outflow tract obstruction.232 The value
of TOE for systematic haemodynamic monitoring in patients at
risk is more controversial. There is no evidence that haemodynamic
monitoring by TOE accurately stratifies risk or predicts outcome.
TOE can be useful in the operating room in patients with severe
valvular lesions. The loading conditions during general anaesthesia
differ from those present in the pre-operative evaluation. Secondary mitral regurgitation is usually reduced during general anaesthesia; on the other hand, primary mitral regurgitation can increase. In
the setting of severe mitral regurgitation, the LVEF overestimates
LV function and other parameters may be more accurate, such as
myocardial deformation obtained by two-dimensional speckle
tracking. More validation is needed before this method can be
used routinely in this setting. In patients with severe aortic stenosis,
appropriate pre-load is important during surgery. Monitoring of LV
end-diastolic volume with TOE may be more accurate than by pulmonary capillary pressure. An appropriate heart rate is crucial in
patients with mitral stenosis and aortic regurgitation: a sufficient
monitor before induction of anaesthesia or institution of a regional

block. The duration of ST-segment changes correlates positively
with the incidence of peri-operative myocardial infarction; 223 therefore, when ST-segment changes occur, the clinician should assume
that myocardial ischaemia is present if the patient has a history of
pre-existing cardiac disease or is undergoing surgery.
It is not clear, however, whether ECG monitoring is sufficiently
sensitive to identify patients with myocardial ischaemia. In addition,
ECG monitoring is of limited value in patients who have intraventricular conduction defects and ventricular paced rhythms. In one study,
Holter recordings were used as the reference standard for detection
of intra-operative ischaemia and the ST-trending monitors were
found to have overall sensitivity of 74% and specificity of 73%.224
The choice and configuration of the leads used for monitoring may
influence the ability to detect significant ST-segment changes. Although V5 has for many years been regarded as the best choice for
the detection of intra-operative ischaemia, one study found that V4
was more sensitive and appropriate than V5 for detecting prolonged
post-operative ischaemia and infarction.225
As many ischaemic events are dynamic and may not always be
detected by the same lead, reliance on a single lead for monitoring
results in a greater risk of failing to detect an ischaemic event. With
the use of selected lead combinations, more ischaemic events can be
precisely diagnosed in the intra-operative setting. In one study, although
the best sensitivity was obtained with V5 (75%), followed by V4 (61%),
combining leads V4 and V5 increased the sensitivity to 90%. When the
leads II, V4 and V5 were used simultaneously, the sensitivity was greater
than 95%.225,226 In another study, in which two or more pre-cordial
leads were used, the sensitivity of ECG monitoring was greater than
95% for detection of peri-operative ischaemia and infarction.225 It
was also shown that ECG monitoring with fewer leads (as few as
three) has lower sensitivity than monitoring with 12 leads and there
is a statistically significant association, independent of peri-operative
troponin values, between peri-operative ischaemia on a 12-lead ECG
and long-term mortality.227,228 Thus, 12-lead ECG monitoring is
recommended especially in high-risk patients, although correct positioning of 12 leads is not feasible in high abdominal and thoracic surgery.
Page 36 of 49
ESC/ESA Guidelines
diastolic period in the former and an appropriatenot longduration of diastole in the latter. When inappropriate control of heart
rate occurs, the consequences should be assessed: changes in transmitral mean gradient and pulmonary artery pressures in mitral stenosis, and changes in LV volumes and indices of LV function in aortic
regurgitation.
Recommendations on intra-operative and/or
peri-operative TOE for detection of myocardial
ischaemia
Recommendations
IIa
230
IIb
230
ECG electrocardiogram; TOE transoesophageal echocardiography.

a
b
Level of evidence.
c
Recommendations on intra-operative and/or

peri-operative TOE in patients with or at risk of
haemodynamic instability
Recommendations
Classa
Levelb Ref. c
TOE is recommended when acute

sustained severe haemodynamic
disturbances develop during
surgery or in the peri-operative
period.
TOE monitoring may be

considered in patients at increased
risk of significant haemodynamic
disturbances during and after highrisk non-cardiac surgery.
IIb
TOE monitoring may be

considered in patients who
present severe valvular lesions
during high-risk non-cardiac
surgery procedures accompanied
by significant haemodynamic
stresses.
IIb
235
TOE transoesophageal echocardiography.

a
b
Level of evidence.
c
Transoesophageal Doppler (TOD) (without echocardiography)

can be also used to monitor cardiac output. A governmentsponsored systematic review performed in the USA concluded
that a strong level of evidence existed to support the usefulness of
TOD in reducing the rate of major complications and the length of
hospital stay after major surgery.233 A similar conclusion was
6.3 Right heart catheterization

Despite more than 30 years experience with the pulmonary artery
catheter (PAC) and right heart catheterization, little evidence
exists in the medical literature to demonstrate a survival benefit associated with PAC in peri-operative patients. A case-control analysis,
carried out in a subset of patients from a large observational study
who underwent PAC placement, and who were matched with a
similar number of patients who did not undergo right heart catheterization, demonstrated a higher incidence of post-operative heart
failure and non-cardiac events than the control group.236
Similarly, a Cochrane review of 12 randomized, controlled clinical
trials studying the impact of PAC in a large spectrum of patientsincluding patients who were undergoing surgery or who were admitted
to the ICU with advanced heart failure, acute respiratory distress syndrome, or sepsisfailed to demonstrate a difference in mortality and
length of hospital stay, suggesting that PAC does not provide information that is not otherwise available to select a treatment plan.237
Routine PAC and right heart monitoring is therefore not recommended in patients during non-cardiac surgery. The use of
other non-invasive peri-operative cardiac output monitoring techniques (including TOE with Doppler monitoring) to optimize cardiac
output and fluid therapy in high-risk patients undergoing non-cardiac
surgery, seems to be associated with reduction in length of stay and
complications,238 yet convincing data on hard end-points are still
lacking.
6.4 Disturbed glucose metabolism

Diabetes mellitus is the most common metabolic disorder in Europe,
with a prevalence of 6.4% in 2010, which is predicted to increase to
7.7% by 2030.239 Type 2 diabetes accounts for .90% of cases, and
is expected to increase, probably due to the obesity epidemic in
children and young adults. The condition promotes atherosclerosis, endothelial dysfunction, activation of platelets, and synthesis
of pro-inflammatory cytokines. According to the World Health
Organization, approximately 50% of patients with type 2 diabetes
die of CVD. It is well established that surgery in patients with diabetes is associated with longer hospital stay, greater use of healthcare resources, and higher peri-operative mortality. Elevated levels
of glycosylated haemoglobin (HbA1c)a marker of poor glycaemic
controlare associated with worse outcomes in surgical and critical care patients.240 Further, surgical stress increases the prothrombotic state, which may present a particular issue in patients
with diabetes; thus diabetes is an important risk factor for perioperative cardiac complications and death. Critical illness is also
characterized by dysglycaemia, which may develop in the absence
of previously diagnosed diabetes, and has repeatedly been
The use of TOE should be considered

in patients who develop ST-segment
changes on intra-operative or
peri-operative ECG monitoring.
The use of TOE may be considered
in patients at high risk of developing
myocardial ischaemia, who
undergo high-risk non-cardiac surgery.
drawn in a separate review commissioned by the UKs National

Health Service (NHS) Centre for Evidence-based Purchasing, performed in three NHS hospitals, with 626 patients being assessed
before- and 621 patients after implementation of an intra-operative
TOD-guided fluid optimization strategy. The findings of the NHS
review showed a 67% decrease in intra-operative mortality, a 4-day
reduction in mean duration of post-operative hospital stay, a 23% reduction in the need for central venous catheter insertion, a 33% decrease in complication rates, and a 25% reduction in re-operation
rate.234
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ESC/ESA Guidelines
hyperglycaemia. In the ICU setting, insulin infusion should be

used to control hyperglycaemia, with the trigger for instigating
intravenous insulin therapy set at 10.0 mmol/L (180 mg/dL) and
relative trigger at 8.3 mmol/L (150 mg/dL). Although there is a
lack of agreement on target glucose range,targets below
6.1 mmol/L (110 mg/dL) are not recommended.240,241
Recommendations on blood glucose control
Recommendations
Post-operative prevention of
hyperglycaemia [targeting levels at
least <10.0 mmol/L (180 mg/dL)]
by intravenous insulin therapy is
recommended in adults after highrisk surgery that requires
admission to the intensive care
unit.
In patients at high surgical risk,

clinicians should consider
screening for elevated HbA1c
before major surgery and
improving pre-operative glucose
control.
IIa
Intra-operative prevention of
hyperglycaemia with insulin may be
considered.
IIb
Post-operative targets <6.1

mmol/L (110 mg/dL) are not
recommended.
III
240,
241
240,
241
HbA1c glycosylated haemoglobin.

a
b
Level of evidence.
c
6.5 Anaemia
Anaemia can contribute to myocardial ischaemia, particularly in
patients with CAD. In emergency surgery, transfusion may be
needed and should be given according to clinical needs. In elective
surgery, a symptom-guided approach is recommended as no scientific evidence is available to support other strategies.
7. Anaesthesia
The optimal peri-operative course for high-risk cardiovascular
patients should be based on close co-operation between cardiologists, surgeons, pulmonologists, and anaesthesiologists. Preoperative risk assessment and pre-operative optimization of
cardiac disease should be performed as a team exercise. Guidelines
on pre-operative evaluation of the adult patient undergoing noncardiac surgery have previously been published by the European
Society of Anaesthesiology.244 The present edition focuses on
patients with cardiovascular risk factors and diseases and also takes
into account more recent developments, as well as peri-operative
management of patients at increased cardiovascular risk.
identified as an important risk factor for morbidity and mortality.240

More recently, the emphasis has shifted from diabetes to hyperglycaemia, where new-onset hyperglycaemia (compared with hyperglycaemia in known diabetics) may hold a much higher risk of
adverse outcome.240,241 Studies in the field of critical care have
demonstrated the detrimental effect of hyperglycaemia, due to
an adverse effect on renal and hepatic function, endothelial function, and immune response, particularly in patients without underlying diabetes. Oxidative stress (a major cause of macrovascular
disease) is triggered by swings in blood glucose, more than by sustained and persistent hyperglycaemia. Minimization of the degree of
glucose variability may be cardioprotective, and mortality may correlate more closely with blood glucose variability than mean blood
glucose per se.240,241
A significant number of surgical patients will have previously undiagnosed pre-diabetes, and are at increased risk of unrecognised
peri-operative hyperglycaemia and the attendant adverse outcomes. Although there is no evidence that screening low- or
moderate-risk adults for diabetes improves outcomes, it may
reduce complications in high-risk adults. Screening patients using
a validated risk calculator (e.g. FINDRISC) can identify high or
very high-risk adults; this can be followed up by screening every
3 5 years with HbA1C.242,243 In patients with diabetes, preoperative or pre-procedural assessment should be undertaken
to identify and optimize comorbidities, and determine the periprocedural diabetes management strategy. For non-cardiac
surgery patients without known diabetes, evidence for strict
blood glucose control is derived largely from studies in critically
ill patients, and is disputed.240,241 Early randomized controlled
trials of intensive insulin therapy maintaining strict glycaemic
control showed morbidity benefits in medical patients in
ICUs, and reduced mortality and morbidity in surgical patients
in ICUs. Subsequent studies, however, found a reduction in
mortality in those whose blood glucose control was less strict
[7.8 10 mmol/L (140 180 mg/dL)] than in those in whom it was
tightly controlled [4.5 6 mmol/L (81 108 mg/dL)], as well as
fewer incidents of severe hypoglycaemia. Subsequent metaanalyses have demonstrated no reduction in 90-day mortality with
intensive blood glucose control but a five- to six-fold incidence of
hypoglycaemia.240,241 Several suggestions have been put forward
to explain the differences in outcome between these studies,
including enteral vs. parenteral feeding, the target for insulin initiation,
compliance with therapy, accuracy of glucose measurements,
mechanism or site of insulin infusion, type of protocol used, and
the nurses level of experience. In addition, there is disagreement
on the timing of the initiation of insulin therapy: tight intra-operative
glucose control may provide benefit but appears to be difficult and,
thus far, studies have mainly been undertaken in patients undergoing
cardiac surgery.
The correlation of poor surgical outcome with high HbA1c suggests that screening patients and improving glycaemic control
before surgery may be beneficial. Although recommendations for
peri-operative management of impaired glucose metabolism are
extrapolated largely from the critical care literature, general consensus is that interventions in the acutely unwell or stressed
patient should be directed towards minimizing fluctuations in
blood glucose concentration whilst avoiding hypoglycaemia and
Page 38 of 49
7.1 Intra-operative anaesthetic

management
7.2 Neuraxial techniques

Spinal or epidural (globally known as neuraxial) anaesthesia also
induces sympathetic blockade. When reaching the thoracic dermatome level 4, a reduction in cardiac sympathetic drive may occur,
with subsequent reduction in myocardial contractility, heart rate,
and change in cardiac loading conditions. The benefit of neuraxial anaesthesia vs. general anaesthesia is much debated in the literature,
with proponents of a beneficial effect of neuraxial anaesthesia and
proponents of the lack of effect on criteria such as mortality or
severe morbidity (myocardial infarction, other cardiac complications,
pulmonary embolism, pulmonary complications, etc.). The same
debate applies to patients with CVDs who must undergo non-cardiac
surgery. Given the continuing debate on this subject we have estimated that neuraxial anaesthesia and analgesia may be considered
for the management of patients with cardiovascular risk factors or
diseases.
One meta-analysis reported significantly improved survival and

reduced incidence of post-operative thrombo-embolic, cardiac,
and pulmonary complications using neuraxial blockade, compared
with general anaesthesia.252 An analysis of a large cohort of patients
undergoing colon resection also suggested improved survival with
epidural analgesia.253 Randomized studies and a meta-analysis of
several randomized clinical trials in non-cardiac surgery patients,
comparing outcomes with regional and general anaesthetic techniques, have shown some evidence of improved outcome and
reduced post-operative morbidity with regional anesthesia.254 256
A recent retrospective analysis, published in 2013, of nearly 400
000 patients undergoing total hip or knee arthroplasty, observed a
significantly lower incidence of major morbidity and mortality in
patients receiving neuraxial anaesthesia.257 The most recent
meta-analysis stated that, when epidurals or spinals were used to
replace general anaesthesia (but not when used to reduce the quantity of drugs required to provide general anaesthesia), there was a significant, 29% decrease in the risk of dying during surgery.10 In both
situations there was a significant decrease in the risk of pneumonia
(55% when replacing general anaesthesia and 30% when decreasing
the requirements of drugs used for general anaesthesia). In both
situations, neuraxial anaesthesia failed to decrease the risk of myocardial infarction. In another recent meta-analysis that targeted patients
undergoing lower-limb revascularization (a category of patients with
risk factors for CVD), there was no difference in mortality, myocardial infarction, or lower-limb amputation between patients allocated
to neuraxial anaesthesia vs. general anesthesia.258 Nevertheless,
neuraxial anaesthesia was associated with a significantly lower risk
of pneumonia.258 Both meta-analyses were based on relatively
small numbers of studies (with a high risk of bias) and patients, and
did not specifically target patients with documented cardiac
disease. Although there are no studies specifically analysing the
changes in outcome related to neuraxial anaesthetic techniques in
patients with cardiac disease, the use of this technique may be considered in patients who do not have a contra-indication after estimation
of risk benefit ratio. Cardiac patients are often on various types of
drugs that interfere with coagulation and care should be taken to
ensure sufficient coagulation ability when neuraxial blocks are
applied.259 Furthermore, combination of general anaesthesia with
thoracic epidural anaesthesia has been shown to statistically increase
the risk of arterial hypotension.260
7.3 Peri-operative goal-directed therapy

There is accumulating evidence underlining the advantages of goaldirected fluid therapy in non cardiac-surgery patients. Goaldirected therapy aims to optimize cardiovascular performance, in
order to achieve normal or even supranormal oxygen delivery to
tissues, by optimizing pre-load and inotropic function using predefined haemodynamic targets. In contrast to clinical signs or arterial
pressure-orientated standard therapy, goal-directed therapy is
based on flow or fluid responsiveness of haemodynamic variables,
such as stroke volume, response to fluid challenges, stroke volume
or pulse pressure variation, or similar cardiac output optimization.
Although goal-directed therapy was initially based on the use of a pulmonary artery catheter, less-invasive techniques have been developed, such as oesophageal Doppler and transpulmonary dilution
techniques, as well as advanced pressure waveform analysis. Early
Most anaesthetic techniques reduce sympathetic tone, leading to a

decrease in venous return due to increased compliance of the
venous system, vasodilatation and, finally, decreased blood pressure;
thus, anaesthesiological management must ensure proper maintenance of organ flow and perfusion pressure. Recent evidence suggests
that there is no universal target blood pressure value to define
intra-operative arterial hypotension, but percentage decreases
.20% in mean arterial pressure, or mean arterial pressure values
,60 mm Hg for cumulative durations of .30 minutes, are associated
with a statistically significant increase in the risk of post-operative
complications that include myocardial infarction, stroke, and
death.104,245,246 Similarly, increased duration (.30 minutes) of
deep anaesthesia (bispectral index scale values ,45) was statistically
associated with an increased risk of post-operative complications.246
Efforts should be made to prevent intra-operative arterial hypotension and inadequately deep anaesthesia.
The choice of the anaesthetic agent has been considered to be of
little importance in terms of patient outcome, provided that vital functions are adequately supported. There is conflicting evidence, stemming from cardiac surgery, over whether a specific anaesthetic agent
is superior in patients with cardiac disease, with the suggestion that
volatile anaesthetic agents offer better cardioprotection than intravenous agents. A meta-analysis published in 2013, combining standard and
Bayesian approaches on studies performed in adult cardiac surgery
patients, concluded that inhaled anaesthesia, as opposed to total intravenous anaesthesia, was associated with a 50% decrease in mortality
(from 2.6% in the total intravenous anaesthesia arm to 1.3% in the
inhaled anaesthetics arm); the Bayesian meta-analysis concluded that
mortality was the lowest when sevoflurane was used as the anaesthetic
agent.247 Comparable data relating to non-cardiac surgery are scarce.
One small study observed a lower incidence of major cardiac events in
vascular surgery patients anaesthetized with a volatile agent than with
an intravenous anaesthetic,248 but two other studies in non-cardiac
surgery patients observed no difference in outcome.249,250
However, the overall incidence of peri-operative adverse events was
too low to be able to address the relationship between choice of anaesthetic agent and patient outcome.251
ESC/ESA Guidelines
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ESC/ESA Guidelines
goal-directed fluid therapyin the right patient cohort and with a

clearly defined protocolhas been shown to decrease postoperative mortality and morbidity.261,262 The mortality benefit of
goal-directed fluid therapy was most pronounced in patients with
an extremely high risk of death (.20%). All high-risk patients undergoing major surgery had a benefit from goal-directed fluid therapy in
terms of complications.263 A meta-analysis published in 2014 demonstrated that, in patients with CVDs, goal-directed therapy decreased
major morbidity without any increase in adverse cardiovascular
events.264
7.4 Risk stratification after surgery

Several recent studies have demonstrated that it is possible to stratify
the risk of post-operative complications and mortality with a simple
surgical Apgar score.265 This post-event stratification might allow
redirecting patients to higher intensity units or selected postoperative measurements of natriuretic peptides and troponin.3,266
Several recent publications have demonstrated that differences

between hospitals, in terms of post-operative mortality, are not due
to the incidence of complications but to the way in which they are
managed.267 These results suggest that early identification of postoperative complications, allied to aggressive management, could decrease post-operative morbidity and mortality. Several recent
meta-analyses have demonstrated that increased post-operative
troponin and BNP concentrations after non-cardiac surgery were
associated with a significantly increased risk of mortality.55,266,268
The prospective Vascular Events In Noncardiac Surgery Patients
Cohort Evaluation (VISION) trial confirmed the results of these
meta-analyses.3 Taken together, these results indicate that early troponin measurement in selected patients could trigger therapeutic consequences. A non-randomized trial demonstrated that a bundle of
interventions aimed at promoting homeostasis was associated with a
significantly decreased incidence of post-operative troponin elevation
and decreased morbidity.269 Pre-operatively and post-operatively,
patients who could most benefit from BNP or high-sensitivity troponin
measurements are those with METs 4 or with a revised cardiac risk
index value .1 for vascular surgery and .2 for non-vascular surgery.
Post-operatively, patients with a surgical Apgar score ,7 should also
be monitored with BNP or high-sensitivity troponin measurements, in
order to detect complications early, independently of their revised
cardiac risk index values.
7.6 Post-operative pain management

Severe post-operative pain, reported in 510% of patients, increases
sympathetic drive and delays recovery.270,271 Neuroaxial analgesia
with local anaesthetics, or opioids and/or alpha2-agonists, and intravenous opioids, alone or in combination with non-steroidal antiinflammatory drugs, seem to be the most effective regimens. The
benefit of invasive (neuraxial) analgesic techniques should be
weighed against potential dangers; this is especially important when
considering the use of neuraxial blockade in patients on chronic
antithrombotic therapy, due to the increased risk of developing a
neuraxial haematoma. A meta-analysis published in 2013, which
Recommendations on anaesthesia
Recommendations
Classa
Levelb Ref. c
Patients with high cardiac and

surgical risk should be
considered for goal-directed
therapy.
IIa
261264
The measurement of
natriuretic peptides and highsensitivity troponin after
surgery may be considered in
high-risk patients to improve
risk stratification.
IIb
3,55,266,
268,272
Neuraxial anaesthesia (alone),

in the absence of contraindications and after
estimation of the riskbenefit
ratio, reduces the risk of perioperative mortality and
morbidity compared with
general anaesthesia and may
be considered.
IIb
10,252257
Avoiding arterial hypotension

(mean arterial pressure <60
mm Hg) for prolonged
cumulative periods (>30
minutes) may be considered.
IIb
104,245,246
Neuraxial analgesia, in the

absence of contra-indications,
may be considered to provide
post-operative analgesia.
IIb
272
Avoiding non-steroidal antiinflammatory drugs (especially

cyclo-oxygenase-2 inhibitors)
as the first-line analgesics in
patients with IHD or stroke
may be considered.
IIb
279
IHD ischaemic heart disease

a
b
Level of evidence.
c
Patient-controlled analgesia is an alternative for post-operative

pain relief. Meta-analyses of controlled, randomized trials have
7.5 Early diagnosis of post-operative

complications
analysed the impact of epidural analgesia vs. systemic analgesia, concluded that epidural analgesia was associated with a significant, 40%
decrease in mortality and a significant decrease in the risk of AF,
SVT, deep-vein thrombosis, respiratory depression, atelectasis,
pneumonia, ileus, and post-operative nausea and vomiting, and also
improved recovery of bowel function, but significantly increased
the risk of arterial hypotension, pruritus, urinary retention, and
motor blockade.272
The transition from acute, post-operative pain to chronic, postsurgical pain is an unfortunate consequence of surgery that adversely
impacts the patients quality of life. The prevalence of chronic postsurgical pain differs in various types of surgery. Limited data suggest
that local or regional analgesia, gabapentin or pregabaline, or intravenous lidocaine, might have a preventive effect against persistent
post-surgical pain and could be used in a high-risk population.273
Page 40 of 49
8. Gaps in evidence
The Task Force has identified several major gaps in the available
evidence:
There is lack of data on how non-cardiac risk factors (frailty,
extreme low or high body mass index, anaemia, immune status)
interact with cardiovascular risk factors and how they impact on
the outcomes of non-cardiac surgery.
There is a need for risk scores that can predict mortality from noncardiac causes.
Interventional or outcome studies need to be performed, that take
into consideration increased pre-operative or post-operative
high-sensitivity troponin, BNP, and other biomarkers.
Areas of uncertainty remain in terms of the optimal type, dose, and
duration of peri-operative beta-blocker therapy in patients undergoing high-risk non-cardiac surgery.
It remains unknown whether or not patients at intermediate surgical risk derive benefit from peri-operative beta-blocker therapy.
Areas of uncertainty remain in terms of the potential benefit of the
introduction of statins in patients undergoing high-risk surgery.
Interventional or outcome studies need to be performed on the
prevention or correction of haemodynamic abnormalities or
low bispectral index values that are statistically associated with
worse outcome.
Information is lacking on the effects of patient status, operating team
size or skills, and the invasiveness of procedures, on outcomes following non-cardiac surgery and these will require investigations in
large, procedure-specific, randomized, multicentre studies.
9. Summary
Figure 3 presents, in algorithmic form, an evidence-based, stepwise
approach for determining which patients benefit from cardiac
testing, coronary artery revascularization, and cardiovascular
therapy before surgery. For each step, the Committee has included
the level of the recommendations and the strength of evidence in
the accompanying Table 8.
Step 1. The urgency of the surgical procedure should be assessed.

In urgent cases, patient- or surgery-specific factors dictate the strategy and do not allow further cardiac testing or treatment. In these
cases, the consultant provides recommendations on peri-operative
medical management, surveillance for cardiac events, and continuation of chronic cardiovascular medical therapy.
Step 2. If the patient is unstable, this condition should be
clarified and treated appropriately before surgery. Examples are unstable coronary syndromes, decompensated heart failure, severe
arrhythmias, and symptomatic valvular disease. Stabilization usually
leads to cancellation or delay of the surgical procedure. For instance,
patients with unstable angina pectoris should be referred for coronary
angiography to assess the therapeutic options. Treatment options
should be discussed by a multidisciplinary expert team, including all
peri-operative care physicians, because interventions might have
implications for anaesthesiological and surgical care. For example,
the initiation of dual anti-platelet therapy after coronary artery
stent placement might complicate locoregional anaesthesia or specific surgical procedures. Depending on the outcome of this discussion,
patients may either proceed for coronary artery intervention, namely
CABG, balloon angioplasty, or stent placement, with the initiation of
dual anti-platelet therapy if the index surgical procedure can be
delayed, or proceed directly for operation with optimal medical
therapy if delay is incompatible.
Step 3. In cardiac-stable patients, determine the risk of the surgical
procedure (Table 3). If the estimated 30-day cardiac risk of the procedure in cardiac stable patients is low (,1%), it is unlikely that
test results will influence management and it would be appropriate
to proceed with the planned surgical procedure. The physician can
identify risk factors and provide recommendations on lifestyle and
medical therapy to improve long-term outcome, as outlined in
Table 8. Initiation of a beta-blocker regimen may be considered
prior to surgery in patients with known IHD or myocardial ischaemia.
Treatment should ideally be initiated between 30 days and a minimum
of 2 days before surgery and should be continued post-operatively.
Beta-blockade should be started with a low dose, slowly up-titrated
and tailored to achieve a resting heart rate of between 60 and 70 bpm
with systolic blood pressure .100 mm Hg. In patients with heart
failure and systolic LV dysfunction, indicated by LVEF ,40%, ACEIs
(or ARBs in patients intolerant of ACEIs) should be considered
before surgery. In patients undergoing vascular surgery, initiation of
statin therapy should be considered. Discontinuation of aspirin
should be considered in those patients in whom haemostasis is difficult to control during surgery.
Step 4. Consider the functional capacity of the patient. If an asymptomatic or cardiac-stable patient has moderate or good functional
capacity (.4 METs), peri-operative management is unlikely to be
changed on the basis of test results, irrespective of the planned surgical procedure. Even in the presence of clinical risk factors, it is appropriate to refer the patient for surgery. The recommendations
for medication are the same as in Step 3.
Step 5. In patients with a moderate or poor functional capacity,
consider the risk of the surgical procedure, as outlined in Table 3.
Patients scheduled for intermediate-risk surgery can proceed for
surgery. In addition to the suggestions above, in patients with one
or more clinical risk factors (Table 4), a pre-operative baseline ECG
is recommended to monitor changes during the surgical procedure.
shown that patient-controlled analgesia has some advantages, with

regard to patient satisfaction, over nurse-controlled or on-demand
analgesia. No difference has been demonstrated with regard to morbidity or final outcome. Patient-controlled analgesia is an adequate alternative in patients not suited to regional anaesthesia. Routines for
follow-up and documentation of effects should be in place.270,274 276
Non-steroidal anti-inflammatory drugs and cyclo-oxygenase-2
inhibitors have the potential for promoting heart and renal failure,
as well as thrombo-embolic events, and should be avoided in patients
with myocardial ischaemia or diffuse atherosclerosis. Recently, an
increased risk of cardiovascular events associated with diclofenac was
detected, specifically in a high-risk population.277 Cyclo-oxygenase-2
inhibitors cause less gastrointestinal ulceration and bronchospasm
than cyclo-oxygenase-1 inhibitors. The final value of these drugs in
the treatment of post-operative pain in cardiac patients undergoing
non-cardiac surgery has not been defined. These drugs should be
avoided in cases of renal and heart failure, or in patients who are
elderly, on diuretics, or those with unstable haemodynamics.278
ESC/ESA Guidelines
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ESC/ESA Guidelines
Step 1
Urgent surgery
Yes
Patient or surgical specific factors dictate the strategy, and do not allow further
cardiac testing or treatment. The consultant provides recommendations on
peri-operative medical management, surveillance for cardiac events and
continuation of chronic cardiovascular medical therapy.
Yes
Treatment options should be discussed in a multidisciplinary team, involving all

peri-operative care physicians as interventions might have implication on
anaesthesiological and surgical care. For instance in the presence of unstable
angina, depending on the outcome of this discussion, patients can proceed for
coronary artery intervention, with the initiation of dual-anti platelet therapy if
the index surgical procedure can be delayed, or directly for operation if delay
is impossible with optimal medical therapy.
No
Step 2
One of active or unstable

cardiac conditions (table 9)
No
Step 3
Determine the risk of the

surgical procedure (table 3)
The consultant can identify risk factors and provide recommendations on

lifestyle and medical therapy, according to the ESC Guidelines.
In patients with one or more clinical risk factors, preoperative baseline
ECG may be considered to monitor changes during the peri-operative
period.
Low
Step 4
Consider the functional

capacity of the patient
> 4 METs
< 4 METs
Step 5
In patients with a poor functional capacity

consider the risk of the surgical procedure
In addition to suggestions above:

In patients with one or more clinical risk factors, non-invasive stress testing
may be considered.
Intermediate
risk surgery
High-risk
surgery
Step 6
Cardiac risk factors (table 4)
In addition to suggestions above:

Rest echocardiography and biomarkers may be considered for evaluation of LV
function and obtaining prognostic information for peri-operative and late
cardiac events
<2
>3
Step 7
Consider non-invasive testing. Noninvasive testing can also be considered

prior to any surgical procedure for patient
counselling, change of peri-operative
management in relation to type of
surgery and anaesthesia technique.
Interpretation of non-invasive
stress test results
Balloon angioplasty:
Surgery can be performed
> 2 weeks after intervention
with continuation
of aspirin treatment.
No/mild/
moderate
stress-induced
ischaemia
Proceed with the planned surgeryb.
An individualized peri-operative management is recommended considering

the potential benefit of the proposed surgical procedure compared with the
predicted adverse outcome, and the effect of medical therapy and/or
coronary revascularization.
Extensive
stress-induced
ischaemia
Bare-metal stent:
>4 weeks after intervention.
Dual antiplatelet therapy
should be continued for
at least 4 weeks.

within 12 months after
intervention for old-generation
DES and within 6 months for
new-generation DES.
CABG
Continuation or discontinuation of aspirin in patients previously treated

with aspirin may be considered in the peri-operative period, and should be
based on an individual decision that depends on the peri-operative bleeding
risk weighed against the risk of thrombotic complications (see also Table 8).
Surgery
a
Treatment should be initiated optimally between 30 days and at least 2 days before surgery and should be continued postoperatively aiming at target resting heart rate of 6070
beats per minute and systolic blood pressure >100 mmHg.
b
For strategy of anaesthesia and perioperative monitoring see appropriate sections.
ACEI = angiotensin converting enzyme inhibitor; CABG = coronary artery bypass graft; DES = drug-eluting stent ECG = electrocardiogram; IHD = ischaemic heart disease;
MET = metabolic equivalent.
Figure 3 Summary of pre-operative cardiac risk evaluation and perioperative management.
In patients with known IHD or myocardial ischaemia, initiation of a titrated

low-dose beta-blocker regimen may be considered before surgery a.
In patients with heart failure and systolic dysfunction, ACEI should be
considered before surgery.
In patients undergoing vascular surgery, initiation of statin therapy should
be considered.
Intermediate or high
Page 42 of 49
Table 8
ESC/ESA Guidelines
Summary of pre-operative cardiac risk evaluation and peri-operative management
Step 6. In patients scheduled for high-risk surgery, consider

non-invasive testing in patients with more than two clinical risk
factors (Table 4). Non-invasive testing can also be considered
before any surgical procedure for patient counselling, or change of
peri-operative management in relation to type of surgery and anaesthesia technique. Risk factors can be identified and medical therapy
optimized as in Step 3.
Step 7. Interpretation of non-invasive stress test results:
patients without stress-induced ischaemiaor with mild-tomoderate ischaemia suggestive of one- or two-vessel diseasecan
proceed to the planned surgical procedure. In patients with extensive
stress-induced ischaemia (as assessed by non-invasive testing),

individualized peri-operative management is recommended,
taking into consideration the potential benefit of the proposed
surgical procedure, weighed against the predicted adverse
outcome. Also, the effect of medical therapy and/or coronary
revascularization must be assessed, not only for immediate postoperative outcome, but also for long-term follow-up. In
patients referred for percutaneous coronary artery intervention,
the initiation and duration of anti-platelet therapy will
interfere with the planned surgical procedure (see sections 4.2
and 4.4).
ACE angiotensin converting enzyme; BNP brain natriuretic peptide; ECG electrocardiogram; IHD ischaemic heart disease; LV left ventricular. Hatched areas: treatment
options should be considered by a multidisciplinary Expert Team.
a
Type of surgery (Table 3): risk of myocardial infarction and cardiac death within 30 days of surgery.
b
Clinical risk factors presented in Table 4.
c
In patients without signs and symptoms of cardiac disease or ECG abnormalities.
d
Non-invasive testing, not only for revascularization, but also for patient counselling, change of peri-operative management in relation to type of surgery, and anaesthesia technique.
e
Initiation of medical therapy, but in the case of emergency surgery, continuation of current medical therapy.
f
Treatment should be initiated ideally less than 30 days and at least 2 days before surgery and should be continued post-operatively, aiming at a target heart rate of 60 70 beats per
minute and systolic blood pressure .100 mm Hg.
g
Unstable cardiac conditions presented in Table 9. Recommendations are based on current guidelines, recommending assessment of LV function and ECG in these conditions.
h
In the presence of heart failure and systolic LV dysfunction (treatment should be initiated at least 1 week before surgery).
i
In patients with known IHD or myocardial ischaemia.
j
In patients undergoing vascular surgery.
k
Evaluation of LV function with echocardiography and assessment of BNP are recommended in patients with established or suspected HF before intermediate- or high-risk surgery in
patients with established or suspected HF (I A).
l
In the presence of American Society of Anesthesiologists class 3 or revised cardiac risk index 2.
m
Aspirin should be continued after stent implantation (for 4 weeks after BMS and 3 12 months after DES implantation).
ESC/ESA Guidelines
Table 9
Unstable cardiac conditions
Myocardial infarction within past 30 days, according to the universal definition49
10. Appendix
Austria, Austrian Society of Cardiology, Bernhard Metzler

Azerbaijan, Azerbaijan Society of Cardiology, Rahima Gabulova
Belarus, Belorussian Scientific Society of Cardiologists, Alena Kurlianskaya Belgium, Belgian Society of Cardiology, Marc J Claeys
Bosnia and Herzegovina, Association of Cardiologists of Bosnia &
Herzegovina, Ibrahim Terzic Bulgaria, Bulgarian Society of Cardiology, Assen Goudev Cyprus, Cyprus Society of Cardiology,
Petros Agathangelou Czech Republic, Czech Society of Cardi-
ology, Hana Skalicka Denmark, Danish Society of Cardiology,

Lone Due Vestergaard Estonia, Estonian Society of Cardiology,
Margus Viigimaa Finland, Finnish Cardiac Society, Kai Lindgren
France, French Society of Cardiology, Gerald Vanzetto
Georgia, Georgian Society of Cardiology, Zurab Pagava
Germany, German Cardiac Society, Malte Kelm Greece, Hellenic Cardiological Society, Costas Thomopoulos Hungary, Hungarian Society of Cardiology, Robert Gabor Kiss Iceland, Icelandic
Society of Cardiology, Karl Andersen Israel, Israel Heart
Society, Zvi Vered Italy, Italian Federation of Cardiology, Francesco Romeo Kyrgyzstan, Kyrgyz Society of Cardiology, Erkin
Mirrakhimov Latvia, Latvian Society of Cardiology, Gustavs Latkovskis Lebanon, Lebanese Society of Cardiology, Georges
Saade Libya, Libyan Cardiac Society, Hisham A. Ben Lamin
Lithuania, Lithuanian Society of Cardiology, Germanas Marinskis
Malta, Maltese Cardiac Society, Mark Sammut Poland, Polish
Cardiac Society, Janina Stepinska Portugal, Portuguese Society of
Cardiology, Joao Manuel Pereira Coutinho Romania, Romanian
Society of Cardiology, Ioan Mircea Coman Russia, Russian
Society of Cardiology, Dmitry Duplyakov Serbia, Cardiology
Society of Serbia, Marina Deljanin Ilic Slovakia, Slovak Society of
Cardiology, Juraj Dubrava Spain, Spanish Society of Cardiology,
Vicente Bertomeu Sweden, Swedish Society of Cardiology, Christina Christersson The Former Yugoslav Republic of
Macedonia, Macedonian FYR Society of Cardiology, Marija Vavlukis
Tunisia, Tunisian Society of Cardiology and Cardio-Vascular
Surgery, Abdallah Mahdhaoui Turkey, Turkish Society of Cardiology, Dilek Ural Ukraine, Ukrainian Association of Cardiology,
Alexander Parkhomenko United Kingdom, British Cardiovascular Society, Andrew Archbold.
The CME text 2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy is accredited by the European Board for Accreditation in Cardiology (EBAC). EBAC works
according to the quality standards of the European Accreditation Council for Continuing Medical Education (EACCME), which is an institution of the European Union of Medical Specialists
(UEMS). In compliance with EBAC/EACCME Guidelines, all authors participating in this programme have disclosed any potential conflicts of interest that might cause a bias in the article.
The Organizing Committee is responsible for ensuring that all potential conflicts of interest relevant to the programme are declared to the participants prior to the CME activities.
CME questions for this article are available at: European Heart Journal http://www.oxforde-learning.com/eurheartj and European Society of Cardiology http://www.escardio.
org/guidelines.
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ANESTHSIE DU CARDIAQUE

POUR CHIRURGIE NON CARDIAQUE

Dan LONGROIS et Jean-Pol DEPOIX

Identifier les patients ayant une cardiopathie comme tant

Donnes pidmiologiques concernant

Incidence des complications > 5 %

Incidence des complications < 5 %

Incidence des complications < 1 %

11catgories de chirurgies, de 0,07% (chirurgie du sein) 5,9%

Donnes pidmiologiques historiques

Donnes pidmiologiques rcentes

Score Apgar chirurgical, daprs [9].

bpm : battements par minute ; PAM : pression artrielle moyenne.

Tableau 40-III Score de risque de complications cardiovasculaires

Antcdents daccident vasculaire crbral

Cratininmie > 2 mg . dL1

Chaque item correspond (hormis la chirurgie) une pathologie existante ou un

Lincidence de ces complications cardiovasculaires graves tait de

Tableau 40-IV Types de cardiopathies propratoires qui ntaient

praticiens lorsquil faut prendre en charge un patient donn avec

Mortalit priopratoire et IDM

14% de complications dans le groupe

Dcs, IDM, ICC,

Complications: 33% RA versus

Anesthsie pridurale; chirurgie

Mortalit priopratoire et IDM

Analyse rtrospective, base de donnes

Dcs, IDM, ICC, TDR,

227 CMO versus

Mortalit priopratoire et IDM

Analyse rtrospective, base de donnes

Ajustement sur type de chirurgie

OR: 1,35 (IC95% : 1,17-1,56),

Lai et al. [98]

Complications : 16,2% IA versus

En analyse multivarie, la mortalit tait

Lai et al. [99]

31 % des patients ont fait des

La survenue dune FA augmente le risque

Lai et al. [100]

ICA (9,7% HTAP versus 0%

En analyse multivarie, une chirurgie en

Les facteurs prdictifs de mortalit taient

Principes gnraux de prise

Tableau 40-VI Situations cliniques qui ncessitent une valuation/prise

Bloc auriculo-ventriculaire de haut degr (Mobitz

CCS : Canadian cardiovascular society ; NYHA : New York heart association.

stable, un cadre de rflexion, de dfinir les meilleures approches

chelle de Duke, daprs [5, 6, 7].

Besoins nergtiques estims selon le type dactivit physique

Se prendre en charge soi-mme pour les activits

Activits sportives importantes (natation, tennis en

Monter un tage sans sarrter

Prise en charge des patients

Lischmie myocardique et les SCA pri-opratoires peuvent

Tableau 40-IX Dterminants de la balance apport/demande

Situation clinique associe

Situation clinique associe

valuation propratoire des patients ayant

Rle de la consultation de cardiologie

Le choix des examens complmentaires pour affiner lestimation

appropris pour diagnostiquer une coronaropathie infraclinique

Tableau 40-XI Performances diagnostiques des principaux examens

Motif spcifique de la demande : ..........................................................................