Choc cardiogénique
juin 2018
Nadia Aissaoui Réanimation médicale
Hôpital Européen Georges Pompidou Université Paris Descartes INSERM-U970, équipe 4
Diplôme d'études spécialisées complémentaires de Réanimation médicale
Plan
1. Definition and profiles
2. Epidemiology
3. Management
Resuscitation and medical therapy
‒ Inotropes/Vasopressors
‒ Revascularisation
‒ New therapies
Mechanical circulatory support
Cardiogenic shock (CS) definition
Established criteria for the diagnosis of CS are as follows:
(1) Systolic blood pressure less than 90 mmHg for 30 min or mean arterial pressure less
than 65 mmHg for 30 min or vasopressors required to achieve a blood pressure ≥ 90 mmHg;
(2) Pulmonary congestion or elevated left-ventricular filling pressures;
(3) Signs of impaired organ perfusion with at least one of the following criteria: (a)
altered mental status; (b) cold, clammy skin; (c) oliguria; (d) increased serum lactate
What are we talking about ? Spectrum of CS
Atkinson TM et al., J Am Coll Cardiol Intv 2016;9:871–83
Various profiles of severity in cardiogenic shock
Inotrope dependent
Sliding on inotropes
Refractory to inotropes
Introduction of inotropes
Various profiles of severity in cardiogenic shock
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When signs of cardiogenic shock remain despite optimal and maximal conventionnal therapy
No consensus about the definition of optimal and maximal conventionnal therapy
Refractory cardiogenic shock
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Refractory cardiogenic shock
– Multicentre, prospective, observational study conducted between 2010 and 2012
– Patients with either acute coronary syndrome (ACS) or non-ACS aetiologies were enrolled within 6 h from detection of CS: n = 219, mean age 67, 74% men
80%
11%
5%
2% 2%
Acute coronary syndrome
Worsening of chronic heart failure
Tako-Tsubo
Myocarditis Others
Etiologies
11 %
6 %
5 %
5 %
1 %
22 %25 %
25 %
,
Other
Post-cardiac arrest resuscitation syndrome
Fulminant myocarditis
cardiotoxic drug intoxication
arrythmia disorders
Pulmonary embolism
Acute myocardial infarction
Acute decompensated heart failure
Cardiogenic shock n=19,416
Etiologies of CS
Medical cardiogenic shock
– acute myocardial infarction
– fulminant myocarditis
– cardiotoxic drug intoxication
– stress-induced cardiomyopathy
– post-cardiac arrest resuscitation syndrome
– decompensated pulmonary vascular disease
– massive pulmonary embolism
– acute decompensated heart failure
Etiologies of CS
Medical cardiogenic shock
Post-surgical CS after heart surgery (including heart
transplantation)
– acute myocardial infarction
– acute decompensated heart failure
– fulminant myocarditis
– cardiotoxic drug intoxication
– stress-induced cardiomyopathy
– post-cardiac arrest resuscitation syndrome
– decompensated pulmonary vascular disease
– massive pulmonary embolism
0
10
20
30
40
50
60
70
1997-1998n=1488
1999-2000n=1760
2001-2002n=2154
2003-2004n=2448
2005-2006n=2518
2007-2008n=2661
2009-2010n=3004
2011-2012n=3383
P<0.001
Mortality of CS patients admitted in ICUs
– In-ICU Mortality during the period study : 47.4% (9 205/19 416) – Decrease : -5,6 % (95% CI, -7,7 to -3,5) from 50.3% (1997-2002) to 44.8% (2009-2012)
Puymirat E et Aissaoui N., EJHF 2016
0
10
20
30
40
50
60
70
80
90
100
1997-1998n=448
1999-2000n=462
2001-2002n=528
2003-2004n=549
2005-2006n=661
2007-2008n=638
2009-2010n=767
2011-2012n=904
0
10
20
30
40
50
60
70
80
90
100
1997-1998n=55
1999-2000n=93
2001-2002n=62
2003-2004n=58
2005-2006n=59
2007-2008n=72
2009-2010n=92
2011-2012n=94
0
10
20
30
40
50
60
70
80
90
100
1997-1998n=221
1999-2000n=240
2001-2002n=266
2003-2004n=268
2005-2006n=249
2007-2008n=286
2009-2010n=343
2011-2012n=420
0
10
20
30
40
50
60
70
80
90
100
1997-1998n=264
1999-2000n=322
2001-2002n=479
2003-2004n=510
2005-2006n=570
2007-2008n=655
2009-2010n=734
2011-2012n=663
Cardiac arrest
Myocardial infarction
Decompensated heart failure
Pulmonary embolism
P=0.85
P<0.001 P<0.001
P=0.009
Mortality according to the primary diagnosis
Puymirat E et Aissaoui N., EJHF 2016
2 main types of medical CS
Severity
Acute etiology of CS ‒ AMI ‒ Fulminant myocarditis ‒ Drug intoxication ‒ ….
INTERMACS 1/refractory CS
INTERMACS 2
High risk for severe forms of CS, even refractory CS
2 main types of medical CS
Severity
Acute etiology of CS ‒ AMI ‒ Fulminant myocarditis ‒ Drug intoxication ‒ ….
Decompensated advanced heart failure
INTERMACS 1/refractory CS
INTERMACS 2
INTERMACS 3/Inotrope dependence
High risk for severe CS, even refractory CS
More often low-out put syndrome Chronic situation
HR 1.11 (0.65-1.91) P=0.69
No cardiogenic shock Cardiogenic Shock
FAST MI 2005 : 3670 pts CS occurred in 224 (6.1%)
Alive at 30D : 3411 with 99 CS
Median follow-up was 525 (inter-quartile range, 305–1496; range, 92–2400) days
Mirabel M et al., Crit Care Med. 2011;39:1029-35
ICU survival : 68%
Long-term survival : 68%
Among 115 patients, 85 patients (75%)
died at 4 months
Circ Heart Fail. 2009;2:320-4
2 main types of medical CS
Severity
Acute etiology of CS ‒ AMI ‒ Fulminant myocarditis ‒ Drug intoxication ‒ ….
Decompensated advanced heart failure
High risk for severe CS, even refractory CS
More often low-out put syndrome Chronic situation
Long term-prognosis
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Sean van Diepen et al. Circulation. 2017;136:e232-e268
“ CS is a hemodynamic problem only at the very beginning, and soon becomes a very complex
disease, with bacterial translocation, overshooting
inflammation and the development of multiple organ
failure”
Combes et al. ICM. 2016
Circulation. 2017;136:e232–e268
Cardiogenic shock management pathway
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Sean van Diepen et al. Circulation. 2017;136:e232-e268
The optimal first-line vasoactive medication in CS remains unclear
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Inotropes or vasopressors ?
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Copyright © American Heart Association, Inc. All rights reserved.
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Copyright © American Heart Association, Inc. All rights reserved.
We have to
improve the
cardiac pump
function
Effects of Inotropes on Microcirculation in CS
Plos One 2014; 9: e103978.
Thirty patients with cardiogenic shock were included
“Levosimendan did not
significantly reduce all-cause mortality at 180
days or affect any secondary clinical
outcomes”
173 deaths (26%)
185 deaths (28%)
– In the SURVIVE study population (1327), 669 (50%) had received b-blockers within 24 h prior to study drug infusion.
Mebazaa A et al., Eur J Heart Fail. 2009;11: 304-11
For patients who used beta-blockers (n = 669), mortality was significantly lower for levosimendan than dobutamine at day 5 (1.5 vs. 5.1% deaths; HR, 0.29; CI 0.11-0.78, P = 0.01).
1. Dobutamine should be used to treat low cardiac output in
cardiogenic shock (strong agreement)
2. Phosphodiesterase inhibitors or levosimendan should not be used firstline (strong agreement)
3. There is a pharmacodynamic rationale for the use of levosimendan in patients on chronic beta-blocker treatment
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Copyright © American Heart Association, Inc. All rights reserved.
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Copyright © American Heart Association, Inc. All rights reserved.
We have to decrease the peripheral vasodilatation
Norepinephrine in cardiogenic shock ?
De Backer D et al., N Engl J Med. 2010;362:779–89
‒ 1679 patients, of whom 858 were assigned to dopamine and 821 to norepinephrine. ‒ The baseline characteristics of the groups were similar.
Plos One 2014; 9: e103978.
Norepinephrine infusion was associated with - no changes in heart rate, - a significant increase in CI, MAP, SVO2, LVEF, dP/dt max, and SVR - a decrease in lactate level
Beurton A et al., Shock 2016; 46; 214-218
12 pigs with AMI and CS : control group (n = 6), norepinephrine infusion (n = 6)
Tarvasmäki T et al., Crit Care. 2016;20:208
‒ The multinational CardShock study prospectively enrolled 219 patients with CS (80% ACS) ‒ Patients with adrenaline : 46 (21%)
Critical care Med, 2011 ;39:450-5.
Critical care Med, 2011 ;39:450-5.
Critical care Med, 2011 ;39:450-5.
Ten patients survived in the epinephrine group and 11 in the norepinephrine-dobutamine group
Critical care Med, 2011 ;39:450-5.
Epinephrine (adrenaline) should be restricted to patients with persistent hypotension despite adequate cardiac filling pressures and the use of other vasoactive agents, as well as for resuscitation protocols
Norepinephrine should be used to restore perfusion pressure during cardiogenic shock (strong agreement)
Epinephrine can be a therapeutic alternative to the combination of dobutamine and norepinephrine, but is associated with a greater risk of arrhythmia, tachycardia, and hyperlactatemia (weak agreement)
‒ « Inotropes, especially those with adrenergic mechanisms, can cause sinus tachycardia, may induce myocardial ischaemia and arrhythmias.
- There is long-standing concern that they may increase
mortality...”
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Copyright © American Heart Association, Inc. All rights reserved.
Sean van Diepen et al. Circulation. 2017;136:e232-e268
Copyright © American Heart Association, Inc. All rights reserved.
Inhibition of systemic
inflammatory response ?
Standard therapy
N = 15
Standard therapy +
LNAM (1mg/kg and 1 mg/kg/h) N = 15
Sean van Diepen et al. Circulation. 2017;136:e232-e268
1.Frequently altered mental status does not ensure correct spontaneous breathing and preservation of the upper airway, two conditions necessary for the appropriate use of NIV 2. It may be cautiously considered in selected CS patients without severe haemodynamic instability
Suggestions for Clinical Practice
The decision to intubate patients with CS should be based on standard critical care criteria; however, clinicians should be both aware of and prepared for the potential hemodynamic deterioration associated with induction therapies, inappropriate ventilation settings, the transition from spontaneous breathing to positive-pressure ventilation, and vagal stimulation association with endotracheal tube placement
In the absence of high-quality data in the CS population, we suggest that MV modes and settings be adjusted to prevent hypoxemia and hyperoxia, to minimize patient discomfort and ventilator dyssynchrony, and to optimize hemodynamics.
Circulation. 2017;136:e232–e268
Circulation. 2017;136:e232–e268
Among patients with CS, a reported 13% to 28% develop acute kidney injury and up to 20% require renal replacement therapy
Patients needing renal replacement therapy were less likely to survive to hospital discharge and had a higher risk of long-term dialysis and mortality
Patients with CS often do not hemodynamically tolerate fluid shifts that can occur with intermittent hemodialysis.
Instead, continuous renal replacement therapy, is more commonly used for those with CS.
Renal Replacement Therapy
Lauridsen et al. Critical Care (2015) 19:452
Acute kidney injury and renal replacement therapy in CS patients
5079 CS patients with 13 % had AKI-RRT
In-hospital mortality :62 % for AKI-RRT patients, and 36 % for non-AKI-RRT patients. (relative risk = 1.70,
95 % confidence interval (CI): 1.59–1.81).
Circulation. 2017;136:e232–e268
The use of percutaneous coronary intervention dereased the
mortality of patients presenting CS after AMI
Aissaoui N, EHJ 2003 33: 2535-43
486 CS patients (1995-2005)
46.7%
22 %
33.6%
40.5%
302 CS patients (1993-1998)
Hochman J, JAMA 2001 33: 190-192
“Intensive care before coronary angiography of CS secondary to MI should be of the “scoop and run” type. What is important is to transfer the patient alive to the
coronary angiography unit without any delay as a result of an attempt at stabilization.”
Multivessel coronary artery : PCI for culprit lesion or all coronary arteries ?
Patients underwent randomization immediately after diagnostic angiography 1:1 ratio
either PCI of the culprit lesion only immediate multivessel PCI
Patients were eligible for the trial if they had acute myocardial infarction with cardiogenic shock
The composite primary end point of death or renal-replacement therapy had occurred in 158 of the 344 patients (45.9%) in the culprit-lesion-only PCI group and in 189 of the 341 patients (55.4%) in the multivessel PCI group
The place of the fibrinolysis in CS STEMI patients ?
“The ESC guidelines (2012) suggest the use of thrombolysis if angioplasty cannot be performed quickly
(within 2 h), with secondary transfer to a center with a coronary angioplasty and cardiac surgery unit”
Circulation. 2017;136:e232–e268
Various profiles of severity in cardiogenic shock
patients
Inotrope dependent
Sliding on inotropes
The most severe form : Refractory to inotropes
Introduction of inotropes
Various profiles of severity in cardiogenic shock
patients
Introduction of inotropes
Introduction of inotropes
‒ « Inotropes, especially those with
adrenergic mechanisms, can cause sinus tachycardia, may induce myocardial ischaemia and arrhythmias.
- There is long-standing concern that
they may increase mortality...”
To minimize the side effects of catecholamines ?
Thiele H, N Engl J Med. 2012 Oct 4;367(14):1287-96.
A patient was considered to be in cardiogenic shock : ‒ systolic blood pressure < 90 mm Hg for more than 30 min
or needed infusion of catecholamines to maintain SBP > 90 ‒ clinical signs of pulmonary congestion, ‒ and impaired end- organ perfusion
Not eligible for the study if ‒ resuscitation for more than 30 minutes; ‒ mechanical cause of CS ‒ onset of shock more than 12 hours before screening;
The IABP does not modify the prognosis of CS
Thiele H, N Engl J Med. 2012 Oct 4;367(14):1287-96.
Randomized prospective study - 300 pts in the IABP group - 298 pts in the control group
39,7 %
41,3 %
• Intraaortic balloon counterpulsation should not be used in cardiogenic shock in the setting of myocardial infarction managed
effectively and quickly by angioplasty (weak agreement).
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. The Impella® Recover LVAD
Reesink et al., Chest 2004, Lemaire A et al., ATS 2014, Seyfarth et al., JACC 2008
‒ Short-term left ventricular support with a flow of 2.5 or 5 l/min (Impella® 2.5 or 5.0, respectively)
‒ A microaxial rotary blood pump is
inserted through the femoral artery and passed retrogradely through the aorta into the left ventricle
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25 patients (n 13 IABP, n 12 Impella LP2.5)
Ouweneel et al. J A C C 2 0 1 7; 69: 2 7 8– 8
On the contrary, due to the limited blood blow obtained with the Impella® 2.5 device, the latter is not recommended for cardiac support during cardiogenic
shock.
Various profiles of severity in cardiogenic shock patients
Introduction of inotropes
No mechanical circulatory support
Various profiles of severity in cardiogenic shock patients
Inotrope dependent
Sliding on inotropes
The most severe form : Refractory to inotropes
Introduction of inotropes
Temporary mechanical circulatory support
Long-term
mechanical circulatory support
INTERMACS 1 and 2 patients
Introduction des inotropes Refractaire aux inotropes
Although there is no strong scientific evidence to support routine MCS therapy in
CS patients to date, it can provide emergency circulatory support while a definite solution is
sought
If temporary circulatory support is needed, the use of peripheral extracorporeal membrane oxygenation is preferred (strong agreement).
Veno-arterial Extra-corporal Membrane Oxygenation
Abrams D et al., J Am Coll Cardiol. 2014;63:2769-78
VA-ECMO provides – both respiratory and cardiac
support, – biventricular support, – is easy to insert, even at the
bedside, – stable flow rates, – and is associated with less
organ failure, after implantation compared to large biventricular assist
Day-30 survival 57 %
Schmidt M et al., EHJ published June 17, 2015
Discharge from hospital 1601 (42%)
N = 235
Reported complication rates were frequent :
- Lower extremity ischemia : 16.9%
- Fasciotomy or compartment syndrome : 10.3%
- Lower extremity amputation : 4.7%
- Stroke: 5.9%
- Major or significant bleeding : 40.8%
- Re-thoracotomy for post-cardiotomy bleeding or tamponade : 41.9%
- Significant infection : 30.4%
When ?
Etiology of CS and
Medical history
Biological data and TTE
Clinical parameters
- Clinical signs associated with rapid deterioration of cardiac function - Treatments administered and tolerance
Which parameters to consider to initiate cardiac support ?
– Liver and renal impairment
– TTE data
Before multi-organ failure
develops
3846 cardiogenic shock patients risk factors associated with mortality: – preexisting comorbidities, – pre-ECMO organ failures, – cardiac arrest, – lower pulse pressure, – lower serum bicarbonate
When to initiate ?
The Impella® 5.0 device can be used in the management of cardiogenic shock
complicating myocardial infarction if the surgical team has experience with its
placement (weak agreement).
– In-ICU survival N = 23 (57%) – D-180 survival – N=20 (50%)
Indications of Impella 5.0 in CS patients
« these systems are currently more expensive and are not adapted to patients with severe biventricular failure. »
Post-heart surgery++++
16 patients developing CS or low cardiac output syndrome after being weaned off cardiopulmonary bypass
Survival to 30 days, 3 months, and 1 year was 94%, 81%, and 75%, respectively
Complications related to Impella devices
Ouweneel DM, et al., JACC 2016
Hemolysis
Complications
Bleeding
Vascular complications
Infections
ECMO or Impella 5.0 ?
Respiratory status Right ventricular function
Surgical availabilities
ECMO and Impella
ECMO ECMO and Impella
Jouan J et al. J Heart Lung Transplant. 2010;29:135-6 Cheng A et al., ASAIO J 2013; 59: 533-6
Various profiles of severity in cardiogenic shock
patients
Inotrope dependent
Sliding on inotropes
The most severe form : Refractory to inotropes
Introduction of inotropes
Decompensated of advanced heart failure
INTERMACS 3/Inotrope dependence
Long-term ventricular assist devices
ESC/EACTS Guidelines on myocardial revascularization. EHJ 2014 Levy et al., Annals of Intensive Care 2015
Management in emergency : Cardiologists, ICU physicians
Timing of cardiac device implantation : Cardiologists, ICU physicians, Surgeons
Implantation-Management : Surgeons, ICU physicians
Decision concerning long-term assist device or heart transplantation :
Cardiologists, Transplant team, ICU physicians, Surgeons
[Tertiary centers]
Mobile Unit of Circulatory Assistance
Management of cardiogenic shock need a team with a
comprehensive, structured, multidisciplinary system of care
Key role of the intensivists
Conclusions
− Several profiles of cardiogenic shock − Major concern : mortality rate around 40 to 60 % at one-month
− Lack of evidence for medical therapy and the choice of inotrope
− Early implantation of MCS without forgetting their complications
− Impella 5.0 assists the LV whereas ECMO is an extracorporeal membrane oxygentation
− Management of cardiogenic shock need a team with a comprehensive, structured, multidisciplinary system of care
Annexes
Other therapies
Corticosteroid Insufficiency in Cardiogenic
Shock Patients
Ducrocq N et al., Shock. 2017 Dec 26.
42%
32%
Corticosteroid Insufficiency in Cardiogenic
Shock Patients : prognostic value ?
Ducrocq N et al., Shock. 2017 Dec 26.
Corticosteroid Insufficiency in Cardiogenic Shock
Patients : prognostic value ?
Ducrocq N et al., Shock. 2017 Dec 26.
Patients with a T0 TC 34 μg/dL or less and Δ max greater than 9 μg/dL appeared to have the most favorable survival (91%)
Corticosteroid therapy was associated with an increased mortality (P = .03)
• Application of hypothermia in non-resuscitated CS patients may also be beneficial from pathophysiological
considerations with multiple beneficial targets