Insuffisance cardiaque aiguë post-opératoire

Alexandre Mebazaa Hôpital Lariboisière,

University Paris 7, U942 Inserm; Paris, France

En résumé ICA post-opératoire

– Se passe en SSPI ou en étage plus tard – Trouver le mécanisme de la décompensation cardiaque

• Dysfonction diastolique du VG • Dysfonction systolo-diastolique du VG • Dysfonction du VD

– ECG, radio du thorax – Biomarqueurs : BNP(ou NT-Pro-BNP)/troponine – Echocardiographie – éviter

• variation de PA et survenue ischémie • Pour le VD : altération de la gazométrie, remplissage excessif

– Favoriser les vasodilatateurs, éviter les catécholamines – ET SURTOUT reprendre vite le(s) traitements au long cours

Il existe 3 types d’IC chronique :

IC chronique avec dysfonction VG systolique et diastolique : bas débit circulatoire

IC chronique avec dysfonction diastolique isolée : OAP

IC droite avec ou sans HTAP

Oedème pulmonaire aiguë

ProblèmeVasculaire Aiguë + Dysfonction Diastolique VG

TOUJOURS

Dyspnée + PAS > 140 mmHg

SK Ghandi, NEJM 2001, 344: 17-22

SK Ghandi, NEJM 2001, 344: 17-22

Pathogénie de l’OAP

• Est un signe de congestion pulmonaire = élévation de la PAPo = POG = PTDVG

• Est un signe de dysfonction diastolique et non systolique SK Ghandi, NEJM 2001, 344: 17-22

Pirracchio et al. Br. J. Anaesth.2007; 98: 707-721

L’oedème aiguë du poumon :

Œdème aiguë du poumon sans état de choc : crise hypertensive, FEVG normale!

VG Normal

12 mmHg

25 mmHg

Volume VG

Ees

HVG + ischémie = compliance VG

diminuée OAP !

Pirracchio et al. Br. J. Anaesth.2007; 98: 707-721

DC ± abaissé Insuffisance ventriculaire droite

IVD

± HTAP

VD

CONGESTION

IT POD

Naija et al AFAR 2009

Décompensation d’une ICC

Dyspnée + PAS <140 mmHg

+

• Gêne respiratoire depuis plusieurs jours

• Elévation du poids • OMI

+ Maladie systémique !

– Insuffisance rénale – Anémie – Hypoalbuminémie

Chaudhry E al. Circulation 2007; 116: 1549-15

ADHF

no ADHF

Daily weight change SAU

CPAP mostly reduces the need

of mechanical ventilation

Peter JV, Lancet 2006;367:1155

Masip J et al. JAMA. 2005;294:3124

Winck JC et al. Crit Care. 2006;10:R69

Blood Gases Evolution

30

50

70

90

110

130

T0 T15 T30 T45

PaO

2

(mmHg)

* *

30

35

40

45

50

55

T0 T15 T30 T45

*

PaCO

2

(mmHg)

« Early CPAP » « Late CPAP »

* p<0,05 CPAP : Early vs Late

Plaisance et al EHJ 2007

Therapy Level of recomm

Level of evidence

Comment

Diuretics I B If fluid retention To reduce dyspnoea

Vasodilators I B (NTG) C (NTP)

Pulmon. congestion Hypertension To reduce dyspnoea

Inotropics agents

II a/b B Hypotension, Hypoperfusion

Therapy and strength of evidence

ESC/ESICM guidelines on AHF; European Heart Journal 2005

Cotter et al. Lancet 1998; 351:389-393

95

Oxy

gen

satu

ratio

n (%

) Nitrates Furosemide

Italy

14%

Spain

14%

UK

13%

Greece

5%

France

12%

Turkey

13%

Germany

12%

Mexico

12%

Australia

5%

ALARM-HF provides a unique view of AHF management across a wide variety of countries

ALARM-HF 9 Countries (4,953 patients)

Mebazaa et al Intensive Care Medicine 2011

inotropes

ALARM-HF: IV treatment at admission

(n=4953)

(n=4167)

(n=1930)

(n=1617)

Effect of IV drugs given during the first 48 hours in AHF patients on in-hospital mortality

Absolute standardized difference (%)

0 20 40 60 80 100

Afib/Acute & ChronicNYHA/No

Periph. valv. dis.Afib/Chron

Afib/Not spec.ACE history

Age/71-80BB pre-hosp

NYHA/IIINYHA/I

Afib/AcuteCreatinine*

Jug. ven. dist.Uric acid*

Coronary artery dis.Sodium*

Age/46-60Secondary AHF

CHFNYHA/IV

Cool extremitiesFemale

De novo AHFAge/61-70

FatigueDyspnoea

LVEF*Heart valve dis.

Age/80>Heart Rate

WeightCadiomyopathy

ObesityPeriph. oed.

Age/15-45NYHA/II

Oxygen sat.*Weight gain

Cardiogenic shockRales

OrthopneaDyslipidemia

DiabetesHypertension

SBPlogit(Propensity)

Pre-matchPost-match

SBP hypertension

Before propensity score match

After propensity score match

IV vasodilatators No IV vasodilatators No

N=1805 N=2362 N=1007 N=1007

Use of vasodilators in

ALARM-HF

Results • IV diuretics and IV vasodilators were started at a median

of 0.5 [0.0 – 1.0] hour and 0.5 [0.0 – 2] hour respectively after admission.

• IV vasodilators were quasi-exclusively nitrates: nitroglycerine in 76 % and isosorbite dinitrate 19 %

• In-hospital mortality: - Before matching 7.6 vs 14.2 % with and without vasoD - After matching 7.8 versus 11 % with and without vasoD

SBP < 100 mmHg (n=318) SBP 100-119 mmHg (n=334)

SBP 120-159 mmHg (n=618) SBP > 160 mmHg (n=694)

Mebazaa et al Intensive Care Medicine 2011

Co-Primary outcome: 30-day all-cause mortality or HF rehospitalization (n=6836)

10.1

4.0

6.1

Hazard Ratio 0.93 (95% CI: 0.8,1.08)

9.4

3.6

6.0

Placebo Nesiritide

HF Rehospitalization

30-day Death/HF Rehospitalization

30-day Death

0

2

4

6

8

10

12

Risk Diff (95 % CI) -0.7 (-2.1; 0.7) -0.4 (-1.3; 0.5) -0.1 (-1.2; 1.0)

%

P=0.31

Hernandez AHA 2010

All Subjects N=6836

Baseline SBP (mmHg) < 123 ≥ 123

N=3346 N=3490

Baseline Ejection Fraction (%)

<40 ≥ 40

N=4362 N=1187

Renal function- MDRD GFR (mL/min/m2)

<60 ≥ 60

N=3395 N=3093

History of CAD No Yes

N=3092 N=3742

History of Diabetes Mellitus No Yes

N=3923 N=2913

-10 -5 0 5 10

30 day death/HF readmission subgroups

Difference (%) and 95% Confidence Interval Risk Difference <0: Favors Nesiritide;

Risk Difference >0: Favors Placebo

Hernandez AHA 2010

30/08/09 26

Absolute standardized difference (%)

0 20 40 60 80 100 120

ObesityAfib/AcuteAfib/Chron

DyslipidemiaCoronary artery dis.

Afib/Not spec.OrthopneaAge/61-70

Afib/Acute & ChronicCHF

DyspnoeaPeriph. valv. dis.Heart valve dis.

NYHA/IUric acid*

RalesFatigue

DiabetesCreatinine*

FemaleHypertension

Sodium*De novo AHF

CadiomyopathyAge/71-80

Jug. ven. dist.BB pre-hospPeriph. oed.

WeightAge/15-45Heart Rate

NYHA/IINYHA/IV

Age/46-60Weight gain

NYHA/NoOxygen sat.*

Age/80>Secondary AHF

ACE historyNYHA/III

LVEF*Cool extremities

Cardiogenic shockSBP

logit(Propensity)

Pre-matchPost-match

After propens

Before propensity score match

After propensity score match

IV inotrope/ vasopressor

No IV inotrope/ vasopressor

No

N=1617 N=3256 N=954 N=954

Use of inotropes/vasopressors

in ALARM-HF

SBP Cardiogenic shock

LVEF

Cool extremities

0 5 10 15 20 25 30

0.0

0.1

0.2

0.3

0.4

0.5

0.6

Days

In-h

ospi

tal m

orta

lity

Whole cohort

Dopamine Dobutamine

Epinephrine

Norepinephrine

Levosimendan

Diuretics

Vasodilatators

Post-discharge treatement after discharge from Acute Heart Failure

0,4

0,5

0,6

0,7

0,8

0,9

1,0

0 30 60 90 120 150 180

Days Since Start of Study Drug Infusion

Prob

abili

ty o

f Sur

vivi

ng LevosimendanDobutamine

Determinants of 180-day All-Cause Mortality

Mebazaa et al. JAMA 2007;297,1883-1891

Acute management CPAP

Inotropes

Post-discharge management Oral beta-blockers ACEI, …

Fig. 2

All-Cause Mortality by Beta-Blocker Useat Baseline and Discharge

0.0

0.6Prob

abili

tyof

sur

viva

l

0 30Days since start of study drug infusion

0.7

0.8

0.9

1.0

60 90 120 150 180

No / No

No / Yes

Yes / Yes

Yes / No

Baseline

Discharge

Fig. 2

All-Cause Mortality by Beta-Blocker Useat Baseline and Discharge

0.0

0.6Prob

abili

tyof

sur

viva

l

0 30Days since start of study drug infusion

0.7

0.8

0.9

1.0

60 90 120 150 180

No / No

No / Yes

Yes / Yes

Yes / No

Baseline

Discharge

M. Boehm et al. Crit Care Medicine 2011

Effects of beta-blockers on patients admitted for acute respiratory failure

Yes/No

No/No

No/Yes

Yes/Yes

Yes/Yes

No/Yes

No/No

Yes/No

CARDIAC CAUSES NON-CARDIAC CAUSES

Noveanu et al Crit Care 2011

Mebazaa et al. Critical Care Medicine, 2008, Suppl 36:129-139

•Non-invasive monitoring (SaO2, BP, temperature) •O2 •Non-invasive ventilation (NIV) as indicated •Physical exam

Management at admission •Lab tests •BNP or NT-pro BNP when diagnosis is uncertain •ECG •Chest X-Ray

Tailored therapy •CS1 (SBP > 140 mmHg): NIV and Nitrates; diuretics are rarely indicated unless volume overload •CS2 (SBP 100-140 mmHg): NIV and Nitrates; diuretics if systemic chronic fluid retention •CS3 (SBP < 100 mmHg): Volume loading with initial fluid challenge if no overt fluid retention; inotrope; PAC if no improvement; if BP fails to improve above 100 mmHg and hypoperfusion persits, then consider vasoconstrictors •CS4 (ACS): NIV; Nitrates; Cardiac catheterization lab, follow guideline recommended management for ACS (aspirin, heparin, reperfusion therapy); IABP •CS5 (RVF): Avoid volume loading; diuretics if SBP >90 mmHg and systemic chronic fluid retention; inotropes if SBP <90 mmHg; If SBP fails to improve above 100 mmHg, then begin vasoconstrictors

Initi

al 9

0-12

0 m

inut

es

•CCU/ICU admission •ECHO if not recently done •Central or arterial line •Additional diagnostic studies •Transfer to tertiary care center

Nex

t 6 –

12

hour

s

Mebazaa et al. Critical Care Medicine, 2008, Suppl 36:129-139

At discharge: Please keep or introduce oral b-blockers etc…

•Non-invasive monitoring • (SaO2, BP, temperature) •O2 •NIV as indicated •Physical exam

Management at admission •Lab tests •BNP or NT-pro BNP •ECG •Chest X-Ray

Treatment Objectives •Decrease dyspnea •Improve well being •Decrease heart rate

•Urine output >0.5 ml/kg/h •Maintain/improve SBP •Restore adequate perfusion

•If dyspnea persists • if SBP <100 mmHg • Organ hypoperfusion • Right ventricular Failure •SaO2 <90% despite O2

•Stay in the ER/Ward

Reassess frequently Clinical and Physical Exam

Treatment Objectives •Decrease dyspnea •Improve well being •Decrease heart rate

•Urine output >0.5 ml/kg/h •Maintain/improve SBP •Restore adequate perfusion •If dyspnea persists • if SBP <100 mmHg

• Organ hypoperfusion • Right ventricular Failure •SaO2 <90% despite O2

•Stay in the ER/Ward

•CCU/ICU admission •ECHO if not recently done •Central or arterial line •Additional diagnostic studies •Transfer to tertiary care center

Reassess frequently Clinical and Physical Exam

Tailored therapy •CS1 (SBP > 140 mmHg): NIV and Nitrates; diuretics are rarely indicated unless volume overload •CS2 (SBP 100-140 mmHg): NIV and Nitrates; diuretics if systemic chronic fluid retention •CS3 (SBP < 100 mmHg): Volume loading with initial fluid challenge if no overt fluid retention; inotrope; PAC if no improvement; if BP fails to improve above 100 mmHg and hypoperfusion persits, then consider vasoconstrictors •CS4 (ACS): NIV; Nitrates; Cardiac catheterization lab, follow guideline recommended management for ACS (aspirin, heparin, reperfusion therapy); IABP •CS5 (RVF): Avoid volume loading; diuretics if SBP >90 mmHg and systemic chronic fluid retention; inotropes if SBP <90 mmHg; If SBP fails to improve above 100 mmHg, then begin vasoconstrictors

Autres nouveautés ?

-Biomarqueurs du diagnostic de l’ICA -Mortalité de l’ICA

Sen

sitiv

ity

BNP (ELISA) QSOX-1 (MS)

0 1

0

1 BNP (ELISA) QSOX-1 (MS)

Sen

sitiv

ity

0 1

0

1

BNP QSOX-1 n = 80 n = 150 n = 80 n = 150

Median AUC 0.84 0.88 0.89 0.86 95% CI 0.74 – 0.92 0.81 – 0.93 0.79 – 0.96 0.79 – 0.92

1 – Specificity 1 – Specificity

Unbaised proteomics: QSOX-1

BNPAUC: 0.88

95%CI: 0.81-0.93

0

1

Sen

sitiv

ity

0 11 – Specificity

Pro-M22AUC: 0.86

95%CI: 0.79-0.92

Previous communication

80 dyspnea patients

Population extended to 150 dyspnea patients

Performance of QSOX-1 in the BNP diagnostic “grey-zone”

0 1

0

1

Pro-M22AUC 0.91

95%CI 0.8-097

BNPAUC 0.58

95%CI 0.42-0.75

BNP ELISA (pg/mL)

Pro

-M2

2 (M

AS

Ste

rcla

ss

TM)

AHFDYSPNEA NON-AHF

Sen

sitiv

ity

1 – Specificity

Diagnostic ‘grey-zone’ of BNP:

100-400pg/mL

Pronota

QSOX-1

0

20

40

60

80

100

1201

98

7

19

88

19

89

19

90

19

91

19

92

19

93

19

94

19

95

19

96

19

97

19

98

19

99

20

00

20

01

20

02

20

03

20

04

20

05

20

06

20

07

20

08

Total F rance

Total G reece

Total F inland

Total S weden

Total S pain

Standardized death rates per 100 000 hab

S Laribi et al.

En résumé ICA post-opératoire

Se passe en SSPI ou en étage plus tard Trouver le mécanisme de la décompensation cardiaque

Dysfonction diastolique du VG Dysfonction systolo-diastolique du VG Dysfonction du VD

ECG, radio du thorax Biomarqueurs : BNP(ou NT-Pro-BNP)/troponine Echocardiographie éviter

variation de PA et survenue ischémie Pour le VD : altération de la gazométrie, remplissage excessif

Favoriser les vasodilatateurs, éviter les catécholamines ET SURTOUT reprendre vite le(s) traitements au long cours