diagnostico shock 2015 12 11 - IMIM · Signosde hipoperfusión tisular conalmenos uno de los...

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13/12/15 1 “Diagnóstico, identificación y selección de pacientes con shock cardiogénico susceptibles de tratamiento avanzado” Barcelona,11 de diciembre 2015 Alessandro Sionis Unidad de Cuidados I ntensivos Cardiolgic os Hospital de la Santa Creu i Sant Pau Barcelona 2 Potenciales conflictos de interés en relación con esta presentación: - Conferencias: Cardiorentis, Novartis, Orion-Pharma - Ensayos clínicos: Cardiorentis, Novartis, Orion-Pharma - Becas: Novartis 3 ¿De Que Estamos Hablando? Hipote nsió n arte ria l p ersist ente ( > 30 min) (P AS < 90 m mHg) o necesidad de fármacos para mantener PAS > 90 mmHg Congestión pulmonar (crepitantes, R3, Rx tórax) Signos de hipoperfusión tisular con almenos uno de los siguientes: (i) Alteración delestado mental (ii) Frialdad de extremidades (iii) Oliguria (< 30 mL /h) (iv) Lactato > 2 mmol/L Disfu nción miocár dica q ue re su lta en la incapacid ad de l cora zón para mant ener un volumen lat id o adec uado a p esar de una precarga normal o elevada

Transcript of diagnostico shock 2015 12 11 - IMIM · Signosde hipoperfusión tisular conalmenos uno de los...

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“Diagnóstico, identificación yselección depacientes con shockcardiogénico susceptibles

detratamiento avanzado”

Barcelona,11dediciembre 2015

AlessandroSionis

UnidaddeCuidados IntensivosCardiolgicos

Hospitalde laSantaCreuiSantPau

Barcelona

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Potenciales conflictos de interés en relación con estapresentación:

- Conferencias: Cardiorentis,Novartis, Orion-Pharma

- Ensayos clínicos: Cardiorentis, Novartis, Orion-Pharma

- Becas: Novartis

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¿DeQueEstamosHablando?

► Hipote ns ión arte ria l p ers ist ente ( > 30 min) (PAS < 90 mmHg) onecesidad de fármacos para mantener PAS > 90 mmHg

► Congestión pulmonar (crepitantes, R3, Rx tórax)

► Signos de hipoperfusión tisular conalmenos uno de los siguientes:

(i) Alteracióndelestadomental

(ii) Frialdaddeextremidades

(iii) Oliguria(<30mL/h)

(iv)Lactato>2mmol/L

► Disfunción miocár dica que re su lta en la incapacid ad de l cora zónpara mant ener un volumen lat id o adec uado a pesar de unaprecarga normal o elevada

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Clinical Presentation AHFEHS-HF II

Nieminen M. Eur Heart J. 2006;27(22):2725-36

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Clinical Presentation AHFEHS-HF II

Nieminen M. Eur Heart J. 2006;27(22):2725-36

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Cardiogenic Shock: Etiology

LVRV

STEMI

NSTEMI

Mechanical complications

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In-hospital MortalityUSIK1995,USIC2000,FAST-MIFranceNationalRegistry

Aissaoui etal.Eur Heart J 2012;33:2535

Deathat30days(%)

7063

8,74,2

0

10

20

30

40

50

60

70

80

1995 2000

Shock NoShock

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The ShockTrial:aRevolution

Mortality in theSHOCKTrial (n=302)

53.3%

66.4%

p< 0.03

Hochman JS.NEJM1999;341:625

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In-hospital MortalityUSIK1995,USIC2000,FAST-MIFranceNationalRegistry

Aissaoui etal.Eur Heart J 2012;33:2535

Deathat30days(%)

7063

51

8,74,2 3,6

0

10

20

30

40

50

60

70

80

1995 2000 2005

Shock NoShock

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In-hospital MortalityUSIK1995,USIC2000,FAST-MIand IABP-II

Aissaoui etal.Eur Heart J 2012;33:2535Thiele H. NEJM 2012;367:1287-1296

Deathat30days(%)

7063

51

40

8,74,2 3,6

0

10

20

30

40

50

60

70

80

1995 2000 2005 2010

Shock NoShock

11Jeger RV et al. Ann Inter Med 2008;149:618- 62 6

Swiss ICU Registry with 23,696 CS patients (1997-2006)

Temporal Trends in CS Incidence

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Incidence according totype ofACS

Awad Hetal.AmHeartJ 2012;163:963-71

Datafrom the Grace Registry (1999-2007)

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Cardiogenic Shock: Etiology

LVRV

Pericardial

Valvular

Arrhythmias

Aortic dissection

Cardiomyopathies

Pulmonary embolism

Pneumothorax

Myocarditis

STEMI

NSTEMI

Mechanical complications

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CardShock Study:Etiology

220patientswithCS

ACS81% non-ACS19%

STEMI 68% NSTEMI 13%

Severelow-outputfailure10%

Other9%

Valvular cause 5%Takotsubo2%Myocarditis 2%

Mechanicalcomplications 9%

Ischemic CMPDilatedCMP

...

Harjola V-Petal.Eur JHeartFail2015;17:501-509

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CardShock study:Mortality

Harjola V-Petal.Eur JHeartFail2015;17:501-509

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Survival CS Patients Treated With ECMO According to Shock Aetiology

KagawaEetal.ESC2015

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OnsetofCardiogenicShock

Awad Hetal.AmHeartJ 2012;163:963-71Jeger RV et al. Ann Inter Med 2008;149:618-626

Datafrom the Grace Registry (1999-2007)

Highest risk subgroups:▶ Older▶ Female

▶ Diabetic▶ Chronic heart failure▶ STEMI▶ Cardiac arrest

► 8.3% of ACS patients develop CS► Vast majority develop CS during hospitalisation (71.5%)?

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ALKKPCIRegistryn=9422 pts→1333 (14.2%)CSInfluence of“symptoms onset tohospital admission” time

LindholmMG.Eur Heart Journal 2003;24:258

43,7 44,954

57,9

0

10

20

30

40

50

60

70

0-3 h 3-6 h 6-12 h 12-24 h

p < 0.001

Identifying Patients atRisk

In-h

ospi

tal M

orta

lity

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19

81,3

59,3

45,7 46,238,6

0102030405060708090

LMS CABG CX LAD RCA

ALKKPCIRegistryn=9422 pts →1333 (14.2%)CSIn-hospital mortality related toculprit vessel

Identifying Patients atRisk

LindholmMG.Eur Heart Journal 2003;24:258

In-h

ospi

tal M

orta

lity

20

37,4

66,1

78,2

0102030405060708090

TIMI 3 TIMI 2 TIMI 0/1

Lindholm MG. Eur Heart Journal 2003; 24:258

ALKKPCIRegistryn=9422 pts →1333 (14.2%)CSPostprocedural TIMIflow gradeandmortality

Identifying Patients atRisk

In-hospitalM

ortality

21Garcia A. Am JCardiol 2009;103(8):1073

Age>75, LMSdisease, LVEF<30%and postprocedural TIMI flowgrade <3

1-ysurvivalw/ourgenthearttrasplantation

Survivalwith

outn

eedforU

HT

Time since admission (days)

83%

19%

6%

Identifying Patients atRisk

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RVDysfunctionRVdysfunctionmay causeor contribute toCS

JacobsAK.J AmColl Cardiol 2003;41:1273

In-hospitaleventsinpatientswithpredominantLVorRVCS

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RVMattersRVinjury not limited toinferiorSTEMI

Masci PG. Circulation 2010;122(14):1405-12

RV involvement33%ininferiorMI RV involvement12%innon-inferiorMI

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RV:Not Only The Heart

RVischaemia

Pulmonarycongestion

RVvolume overload

Tricuspidregurgitation

↑RightsidedFilling pressures

Venous congestion

LVischaemia

Ventriculardipendence

↑Renalinterstitial pressure ↑intra-abdominalpressure

↑Neurohormonal activation

↑SVR

↓CO

↓Organ perfusion

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25Ince C.Crit CareMed1999;27:1369-1377

Microcirculation

UltimatetherapeuticgoalinCSis torestoremicrocirculatoryfunction(adequateoxygensupplytosustaincellularfunction)

Active recruitmentof microcirculationisessentialOrthogonalpolarisation spectral(OPS) imaging allowsdirect visualizationof sublingualmicrocirculation

26SpronkPE.Lancet2001;360:1395-1396

Microcirculation

Orthogonal polarisation spectral imaging (OPS)

Microcirculatory shutdown

► Increased oxy gen consumption andimpaired oxygen deliv ery andextraction due to microcirculatoryshutdown and shunting

Before and after nitroglycerin

Duringsepsis (andCS) microvasculatureisthef irsttogoandthelasttorecover

27denUil CA.Eur HeartJour2010;31:3032-3039

Microcirculation

Sublingual perfused capillary density measured with sidestream dark-field imaging

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28denUil CA.Eur HeartJour2010;31:3032-3039

Microcirculation

29denUil CA.Eur HeartJour2010;31:3032-3039

SurvivalstratifiedaccordingtoquartileofbaselinesublingualPCD

Predictors of 30-day mortality

Microcirculation

30Prondzinsky Retal.Crit CareMed2010;38:152–160

APACHEIIScoreandMortalityIABPShockTrial

p<0.05

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31Prondzinsky Retal.Crit CareMed2010;38:152–160

BNPandMortalityIABPShockTrial

p=NS

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Survival according to NT-proBNP

Jarai R.etal.Crit CareMed2009;37:1837

Biomarkers: Natriuretic Peptides

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Admission lactateand30-daymortality(1997-2007)

Vermeulen et al.Critical Care2010;14:R164

Biomarkers:Lactate

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30-daysurvivalafterPCIaccordingtolactatelevels(>1,8mmol/L)

Vermeulen et al.Critical Care2010;14:R164

Biomarkers:Lactate

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AUC for 90-day mortality for lactate and ADM

Biomarkers: Adrenomedulin

0,6

0,65

0,7

0,75

0,8

0,85

0h 12h 24h 48h 72h 96h 5-10 days

Lactate ADM

Time from baseline

AUC

Tolppanen H, Rivas-Lasarte M et al. Unpublished data

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90-day survival curves for lactate and ADM

Biomarkers: Adrenomedulin

Tolppanen H, Rivas-Lasarte M et al. Unpublished data

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37Prondzinsky Retal.Crit CareMed2010;38:152–160

CIandMortalityIABPShockTrial

p=NS

38Fincke Retal.J AmColl Cardiol 2004;44:340–8

0.60(0.44,0.83)P<0.002

CardiacPowerOutput(CPO)andCPIndex(CPI)

(W)=MAPxCO

► CouplesPressure(MAP)andFlow (CO)=CardiacPumping

► Cutoff0.53W(PPV56%;NPV78%).)

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Predictors of In-Hospital Mortality

Harjola V-Petal.Eur JHeartFail2015;17:501-509

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CardShock Risk Score

Harjola V-Petal.Eur JHeartFail2015;17:501-509

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Performance compared to otherscores in derivation and validationcohorts

Harjola V-Petal.Eur JHeartFail2015;17:501-509

42Thiele et al. EAPCI Textbook 2012; Chapter 23

Medical txInotropic support

Vasopressor supportFluids

Ventilatory supportIABP ?

Revascular ization

LVAD / ECMO Weaning

Assess neurological & end-organ dysfunction

Standard tx

Consider surgical LVAD / BiVAD

Destination tx Heart trasplantation

Patientunstable

Patientstable

Weaning

Weaning

Recovery ofcardiac function

No recovery ofcardiac function

Impaired Normal

Age, comorbidities? Age, comorbidities?

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Gaps In Knowledge

► Definition of pre-shock

► Definition of refractory shock

► Best approach to MVD (CVLPRIT-SHOCK ongoing)

► Myocardial protection strategies

► New biomarkers for early diagnosis of end-organ damageand risk stratification

► New pharmacological therapies

► Treatment of SIRS

► Equipoise in access to best treatment

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Equipoise in Access to Treatment in CS

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¡Necesitamos Un Consenso Sobre Redes de Atención al Shock Cardiogénico!

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[email protected] at

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