Prise en charge

du choc cardiogénique
en dehors de la revascularisation

Ivan LAURENT
Institut Hospitalier Jacques Cartier
Massy
Qu’est-ce qu’un choc cardiogénique?
THEORICIEN CLINICIEN
–HypoTA persistante
–Bas-débit cardiaque (PAS < 90 mmHg > 30 min)
–⇒ hypoperf. tissulaire – + signes d’hypoperf périph.
–malgré un (↓ vigilance, extrémités
volume intra-vasc. fraîches, oligurie)
adéquat – ∅ réponse remplissage vasc.
– + doc. dysfonction
myocardique

HEMODYNAMICIEN
–IC < 2.2l/min/m²
–PAPO > 18 mmHg
–RVSI > 1800-2000 dynes.s/cm5
 Etiologies du choc cardiogénique
Choc cardiogénique

Infarctus du myocarde Autres conditions

Autres atteintes
Altération sévère Ischémie-reperfusion
myocardique myocardiques
de la contractilité
•CMD
•CEC prolongée
•IDM > 40% •Myocardites
•Choc septique
•IDM sur ↓ de la FE VG •Contusions myocard.
« hypokinétique »
•Extension/Récidive
•Sidération myocardique Obstacles «gauches»
d’IDM
post-ACR
•A l’éjection (RA, CMO)
Complications
•Au remplissage (RM,
mécaniques
Altérations myxome)
•IM sur rupture de pilier
de la FC Régurgitations valv.
•CIV post-IDM
•TV •IAo
•Rupture paroi libre
•BAV •IM (rupture cordage)
Infarctus extensif
du VD
 Epidemiology of cardiogenic shock
following AMI

• Incidence: 7.5% with

conservative strategy

• Recent studies: 3-7%

• >50% patients develop shock

24-48 hours after admission

• Overall mortality: 80%

 Quand rencontrerai-je
H0
un choc cardiogénique ?
H 1.8 H6 H 22 H 38 H 94

H
H 100 %
75 %
50 % 7.2 %
25 %
(GUSTO I)
0%
Sus-décalage ST

H
25 % 50 %
Sans ST+ 2.9 %(PURSUIT)
 The downward spiral
in cardiogenic shock
Myocardial dysfunction
Systolic Diastolic

↓ cardiac output ↑LVEDP

↓ stroke volume Pulmonary congestion

↓ systemic Hypotension
perfusion
↓ coronary perfusion Hypoxemia
pressure

Compensatory
vasoconstriction, Ischemia Progressive
fluid retention myocardial
dysfunction

Hollenberg SM, et al. Ann Intern Med 1999; 131: 47-59

Death
Reperfuser
Coûte que coûte
 The SHOCK trial:
« A positive view of a negative trial »
SHOCK Trial

Optimal medical management Agressive revascularisation strategy

including thrombolysis and IABP with PTCA and/or CABG

N=150 N=152 RR, P

30-day -9.3%, p=0.11

56.0% 46.7%
Mortality
Age <75 56.8% 41.4% -15.4%, p=0.02

6-months
63.1% 50.3% -12.8%, p=0.027
Mortality

Hochman JS, et al. N Engl J Med 1999; 341: 625-34

Cardiac failure is the first cause of death
after PTCA for AMI
n= 98

Pump Failure
Reinfarction
Myocardial rupture
Arrhythmia 40
Other cardiac death 30
Stroke 20
Anoxic encephalopathy
10
Procedure related deaths
0
0 3 6 9 12 15 18 21
Day of death
Brodie BR, et al. Am J Cardiol 1997; 79: 1586-91
Eliminer une complication mécanique
imposant la chirurgie en urgence
 Mechanical complications of AMI
diagnosed by TEE

LA

RV
LV

LV Ao

Acute mitral regurgitation Ventricle septal defect

associated with papillary muscle rupture
How to take care of a « VIP »

« Ventilation, Infusion, Pump »

Weil MH, et al. JAMA 1969; 207:337

Imbalance of O2 demand / delivery
in cardiogenic shock
↓O2 supply
↓ Coronary Blood
Flow
↓ diastole

Hypoxia
↑ O2 demand
Tachycardia
↑ Wall stress

↑Respiratory
muscle VO2
Respiratory muscle fatigue leading to apnea
during cardiogenic shock
n= 13 dogs (spontaneous ventilation)
15

10

0
C 30 60 90 120 150
Time (min)
VE (l/min) Pdi (cmH2O)
Aubier M, et al. Am J Physiol 1981; 51:499-508
 Cardiovascular effects of hypoxemia
120
in animal models

21%
11.9%
Pressure (mmHg)
60
0

0 20 40
Volume (ml) above baseline
Walley KR, et al. Circ Res 1988; 63:849
Cardiovascular effects of respiratory acidosis
in animal models

150
Eucapnia
Hypercapnia
β- Eucapnia
LV Pressure (mmHg)

β- Hypercapnia
100
50
0

0 20 40

LV Volume (ml)
Walley KR, et al. Circ Res 1990; 67:628
 Hemodynamic benefit of mechanical
ventilation
in cardiogenic shock

Normal Decreased contractility

R
LV pres sure (mmHg)

PV

LV pressure (mmHg)
ES

R
↓ ITP

PV
ES
↓ LV ejection
pressure
↓ LV ejection
pressure ↑ ITP
↑ ITP

↓ LV preload
↓ LV preload

LV volume (ml) LV volume (ml)

From Pinsky MR. Intensive Care Med 1997; 23: 493-503
IABP + mechanical ventilation with PEEP
vs IABP alone in cardiogenic shock
P=0.04 P=0.01
100

75

50

25

0
IABP Weaning Hospital discharge
IABP alone (n= 18) IABP + MV (n=10)

Kontoyannis DA, et al. Intensive Care Med 1999; 25: 835-8

 Ventilation during cardiogenic shock
in clinical practice
• C-PAP (5-10 cmH2O):
– Congestive heart failure rapidly responsive to Dobutamine
– Hypocapnic / Normocapnic pulmonary oedema
– No marked acidosis , neither encephalopathy
• Boussignac’s system:
Ventilation during cardiogenic shock
in clinical practice
• Non Invasive Ventilation
– Congestive heart failure rapidly responsive to Dobutamine
– Hypercapnic / Normocapnic pulmonary oedema
– No marked acidosis , neither encephalopathy
Ventilation during cardiogenic shock
in clinical practice

• Indications for mechanical ventilation:

– Shock requiring epinephrine
– Acute respiratory failure before PTCA
– Respiratory acidosis or uncompensated metabolic
acidosis
– Altered mental status
Sedative drugs for cardiogenic shock
in clinical practice

• Induction anesthesia
– Etomidate 20 mg + Midazolam 2mg +
Vecuronium 10mg IV

• Maintenance of anesthesia
– Midazolam 5mg/h IV + Fentanyl 100 mcg/h
– Curare agent for paralysis as required
 Preload must be increased
during low cardiac outputs

Normal volume
Normal contractility
Increased preload
Normal preload
Depressed contractility
Increased preload
OUTPUT

VASCULAR LOAD

Shoemaker’s Text Book of CritIcal Care, 1995

 Each patient owns its optimal PAOP
following acute myocardial infarction

Survivors
4.0
Non survivors
CI (L.min-1.m²)

2.1
2.0

10 18 20 30 40
PAOP (mmHg)
Forrester JS, et al. N Engl J Med 1976; 295: 1356
 Fluid challenge monitored
by Continuous Cardiac Output

Vol expansion 250 cc 500 cc 500 cc 1000 cc

3.2 3.5

3.0
CI
2.5

2.0
13:00 13:15 13:30 13:45 14:00 14:15 14:30

PAOP 20 19 21 22 22
Hemodynamic management of cardiogenic
shock in clinical practice

• Fluid challenge unless severe pulmonary

edema

• PAS> 80 mmHg: Dobutamine: 10-15 mcg/kg/min

• PAS< 80 mmHg: Dopamine: 10-15 mcg/kg/min

• If unresponsive: Epinephrine infusion

 Medical Management of cardiogenic shock
in practice

General
Anesthesia
Volume loading+
PAM <65
Acute respiratory
Mechanical
SHOCK failure
ventilation +
Encephalopathy PEEP
Dobutamine 10-15
Volume loading++

Consider
epinephrine
Transfer to PCI center
 VIP for cardiogenic shock
in clinical practice

5 10 Days

Mech.Ventilation Weaning
V
SHOCK

Volume expansion Volume depletion

I

Catecholamines Discontinuation
P
IABP
ACE inhibitors
 How to monitor a VIP

V…, Ischemia, Pulse oxymetry

12 lead Electrocardiogram Monitoring

•General Electric
•Datascope
•Siemens
 Le ST, plus puissant facteur
de complications en post-infarctus

Major Adverse coronary events X² P RR 95%

↓ ST >50% ST segment res. 8.4 0.004 3.4 (1.5–7.9)

Shock 3.7 0.06

↓ ST < 50%
Multivessel dis. 3.2 0.07

TIMI grade 2.5 0.11

Age 2.2 0.14

Cholesterol 2.2 0.13

Claeys et al. Circulation 1999; 99: 1972-77

 Masimo Pulse oxymetry
as a gold standard for acute monitoring
Motion and Low Perfusion Study

Barker SJ. Anesthesia and

Analgesia 2002;94(S1):S17-
21.
Oximeter SpO2 SpO2 SpO2 Drop Out
Sensitivity Specificity Performance Index
99% 97% 93% 0.0%

Philips/HP CMS B.0 70% 83% 80% 3.7%

Nellcor N-395 70% 73% 73% 4.0%
Datex-Ohmeda 3900 60% 52% 68% 1.0%
Novametrix MARS 40% 42% 58% 2.4%
Nellcor N-295 39% 53% 55% 7.8%

• Masimo SET oximeters detect approximately 10 times more true events than any "Next Generation"
pulse oximeter.1
• Masimo SET oximeters have one-tenth the false hypoxemia alarms of "Next Generation" pulse
oximeters.1, 2, 3, 4
Un zeste d’inflammation…

… qui peut faire mal

 TNF-α levels in patients
with class I-IV heart failure

10
TNF a (pg/mL)

8
6
4
2
0
Control I II III IV
NYHA Functionnal Class
Systemic inflammation in patients
with cardiogenic shock
ng/mL pg/mL
200 600

150
400
100
200
50

0 0
Controls (n=7) Cardiogenic Septic shock
shock (n=7) (n=15)
TNF a TNF 2r IL-6
De WERRA I, et al. Crit Care Med 1997; 25: 607-13
 The cytokine hypothesis

TNF-α
IL-6
↑ LV size
Stretch
↓ LV Function

?
? Immune
activation

KAPADIA S , et al. Cardiol Clin 1998; 16: 645-56

Do all nonsurvivors of cardiogenic shock die
with a low Cardiac Index?

LIM N, et al. CHEST 2003; 124:1885–1891

The downward spiral in cardiogenic shock:
« expanding the paradigm »

1. Mean LV EF is only moderately severely

depressed (30%), with a wide range of EFs and
LV sizes noted.
2. SVR on vasopressors is not elevated on average,
with a very wide range of SVRs measured.
3. A clinically evident systemic inflammatory
response syndrome is often present in patients
with CS.
4. Most survivors have class I CHF status.
HochmanJS.Circulation 2003; 107: 2998-3002
The downward spiral in cardiogenic shock:
« expanding the paradigm »

Systemic Myocardial dysfunction

inflammation
Systolic Diastolic
↑inflammatory ↓ cardiac output ↑LVEDP
cytokines ↓ stroke volume Pulmonary congestion

↑iNOS ↓ systemic Hypotension

perfusion
↓ coronary perfusion Hypoxemia
↑NO pressure
↑Peroxynitrite Compensatory
vasoconstriction, Ischemia Progressive
fluid retention myocardial
vasodilation dysfunction
↓ SVR
Death

Hochman JS. Circulation 2003; 107: 2998-3002

Comme disait ma grand-mère…

« Deux ou trois claques sont excellentes

pour faire circuler le sang! »
 Le grand espoir du LNMMA…
• Critères d’inclusion:
– Infarctus en phase aiguë;
– Artère coupable
perméable;
– Choc cardiogénique
« réfractaire » < 24 heures
associant:
• Signes d’hypoperfusion
périphérique TRIUMPH Trial
• PAS < 100 mmHg
• Malgré vasopresseurs (Dopa,
N Ad, Adrénaline)
– Critères hémodynamiques Tilarginine Placebo
• Pressions gauches élevées Bolus 1.0 mg/kg IV

• FE < 40 % perfusion 1.0mg/kg/h (5h)

N=201 N=180

The TRIUMPH Investigators, JAMA. 2007;297:1657-1666

 …Tombe à l’eau
avec un dur retour à la réalité

58 %
59 %

The TRIUMPH Investigators, JAMA. 2007;297:1657-1666

 Au revoir le GIK
CREATE-ECLA
Randomization of 20.201 Pts

• « In this large, international

randomized trial, high-dose GIK
infusion:
had a neutral effect on mortality
cardiac arrest, and cardiogenic
shock in patients with acute
STEMI. »

The CREATE-ECLA Trial Group Investigators JAMA. 2005;293:437-446

Perdus dans le labyrinthe
de l’inflammation:
Savoir prendre un peu de hauteur…
 Ischémie-reperfusion

Xanthine
Peroxydation oxydase Production de radicaux
lipidique libres


Lésions cellulaires Protéases Adhésion/migration des
endothéliales PNN

Voie de NOs Voie du TX Activation du Cytokines Expression des moléc.

↓NO ↓PGI2
Cpt IL-1, 
IL-6,
d’adhésion
C3a, C5a  IL-8, 
TNFα ICAM-1, ICAM-2, ELAM
↑ Endothéline  ↑TxA2
↑LTB4
↑PAF

Vasoconstriction Chimiotactisme PNN activés exprimant les

 Agrégation plq des PNN intégrines CD11/CD18

 Démontré expt et/ou clint dans l’ACR

D’après GRACE. Br J Surg 1994; 81: 637-47
 Continuous hemofiltration
for the failing heart

Liquide de
réinjection

TNF-α
IL-6
C3a, C5a Ultrafiltrat

Coraim FI, et al. New Horizons 1995; 3: 725-31

Early Hemofiltration (HV-HF) improves survival
after resuscitated cardiac arrest
Kaplan-Meier survival estimates. by groupe
Survival A / B / C : 45 % / 45 % / 26%
1.00
Survival duration (days)
days) : A : 26 (10 - 60)
B : 15 (8 - 60)
C : 6 (5 - 60)
p < 0.05
0.75

groupe A
0.50
groupe B

0.25 groupe C

0.00
0 20 40 60
analysis time (day)

Haz. Ratio for death p 95%CI

Before CPR (/mn) 1.1 0.14 0.96-1.35

Duration CPR (/mn) 1.1 0.01 1.01-1.14
Asystole 1.6 0.51 0.37-6.4
HF 0.25 0.049 0.06-0.99
LAURENT I, et al. J Am Coll Cardiol 2005; 46: 432-7
 Hypothermie thérapeutique
Expérience clinique au décours de l’ACR
Survie hospit./ à 6 mois
• 2 Etudes randomisées 60 P= 0.046 P= 0.02

• Patients:
– Total: 352 40
– ACR d’origine cardiaque
– Rythme initial: FV
– Coma persistant
– Hémodynamique stable
20

• Induction d’une hypothermie

modérée (32-34°C)
– Moyens externes 0
– Durée: 12 à 24 h Et. Austral. Et. Europ.
n= 77 n= 275
Hypothermie Contrôle
• Pas d’effet secondaire notable
N Engl J Med 2002; 346: 549-
549-56 et 557-
557-63
The time for mechanical circulatory
support
 The time for mechanical circulatory
support
Usual Contraindications
Criteria selection •Age > 70
•CI < 1.8 l/min/m² •Renal Failure
•SBP< 90 mmHg •Cerebrovasc. Insufficiency
•LVEDP > 20 mmHg •Hepatic failure
•Urine output < 20 ml/h •Coagulopathy
•SVR > 2100 dyne.s.cm-5 •Sepsis
•Metabolic acidosis •Metastatic cancer
•Adequate preload with
maximum inotropic/ IABP
support
Broderick TJ, et al. In Shoemaker ’s Textbook of Crtical Care (1995)
Assistances circulatoires
« crédibles » en salle de cathétérisme

ISAR-SHOCK Trial
26 pts cardiogenic shock

Percutaneous LVAD IABP

Impella LP 2.5

N=12 N=13

Delta CI: Delta CI:

0.49+/-0.46 P: 0.02 0.11+/-0.31
l/min/m² l/min/m²

30 days mortality: 46 % (p: ns)

Seyfarth M, et al. J Am Coll Cardiol. 2008;52(19):1584-8.

Assistances circulatoires
« crédibles » en salle de cathétérisme

Impella Tandem Heart

Thiele H, et al. European Heart Journal (2007) 28, 2057–2063

 Conclusion
• Perfect reperfusion is the key treatment

• Early death can occur despite successful PTCA

• Take care of a VIP…

• Mechanical support as a « bridge to graft /

recovery » must be discussed early