Download ICU management: special cases of cardiogenic shock.

ICU MANAGEMENT:
SPECIAL CASES OF
CARDIOGENIC SHOCK
Maria Rosa Costanzo, M.D., F.A.C.C., F.A.H.A.
Medical Director, Midwest Heart Specialists-Advocate Medical Group
Heart Failure and Pulmonary Arterial Hypertension Programs
Medical Director, Edward Hospital Center for Advanced Heart Failure
Presenter Disclosures
Employee of: Midwest Heart Specialists-Advocate medical Group
Consultant to: Gambro, Medtronic, St. Jude Medical, Sorbent
Speaking Honoraria: Gambro, St. Jude Medical
Research Grants to the Midwest Heart Foundation: Gambro, St.
Jude Medical, United Therapeutics, Gilead, Impulse Dynamics
Causes of Cardiogenic Shock
Acute Myocardial Infarction
Pump Failure
Large MI, generally involving ≥ 40% of LV
Smaller MI with pre-existing LV dysfunction or a prior MI
MI extension or expansion
Reinfarction
Mechanical Complications
Acute MR due to rupture of a papillary muscle or chordae tendinae or severe papillary muscle dysfunction
VSD caused by rupture of the interventricular septum
LV free wall rupture
Pericardial tamponade due to rupture of the LV free wall or hemorrhagic pericardial effusion
RV infarction
Other Conditions
End-stage CM
Myocarditis
LVOT obstruction
AS
HOCM
Obstruction to LV filling
MS
LA myxoma
Acute MR (chordal rupture)
Acute AR
Myocardial contusion
Prolonged CPB
Hollenberg SM et al. Ann Intern Med 1999; 131:47
Treatment Options for Cardiogenic Shock Due to LV Dysfunction
General Measures
Ventilatory support to correct hypoxemia and, in part, acidosis
Optimize intravascular volume
Sodium bicarbonate only for severe metabolic acidosis (Ph < 7.10-7.15)
Aspirin
IV heparin
Possible glycoprotein IIb/IIIa inhibitor with NSTEMI
PA catheter
Specific measures
Pharmacologic Support
Sympathomimetic inotropes (dopamine)
Norepinephrine (for refractory hypotension)
Mechanical Support
IAPB combined with PCI or CABG or possible thrombolytic therapy
Newer Devices
LV or BIV cardiac assist devices
Percutaneous CPB
Reperfusion/Revasc.
Primary PCI
CABG
Thrombolytic therapy for pts. not receiving PCI in a timely manner
Hemodynamic Profiles of Shock Types
Physiologic
Variable
Preload
Pump
Function
Afterload
Tissue
Perfusion
Clinical
Measurement
PAWP
CO
SVR
Hypovolemic
↓
↓
↑
Mixed
Venous
Oxygen
Saturation
↓
Cardiogenic
↑
↓
↑
↓
Distributive
↓ or ↔
↑
↓
↑
Relative Potency of
Commonly Used Vasoactive Agents
Cardiac
Drug
Peripheral Vascular
Dose
Heart
Rate
Contractility
Vasoconstriction
Vasodilatation
Dopaminergic
2-40 mcg/min
+
++
++++
0
0
Dopamine
1-4 mcg/Kg/min
+
+
0
+
++++
Dopamine
4-20 mcg/Kg/min
++
++ to +++
++ to +++
0
++
1-20 mcg/min
++++
++++
++++
+++
0
Phenylephrine
20-200 mcg/min
0
0
+++
0
0
Vasopressin
0.01-0.03 U/min
0
0
++++
0
0
Dobutamine
2-20 mcg/Kg/min
++
+++ to ++++
0
++
0
0.375-0.75 mcg/Kg/min
+
+++
0
++
0
0.05-0.2 mcg/Kg/min
+
+++
0
++
0
Norepinephrine
Epinephrine
Milrinone
Levosimendan
Hollenberg SM, Parrillo JE 2010
α- and β-Adrenergic Effects of
Vasoactive Catecholamines
β
Pressure
Isoproterenol
Dopexamine
Dobutamine
Dopamine
Epinephrine
PE NE Dopa Epi Dobut Dopex Iso
Norepinephrine
Phenylephrine
α
α
β
Staging of Acute Kidney Injury
RIFLE Stage
RISK
GFR or sCr Criterion
Urine Output
↑ sCr x 1.5
<5 ml/Kg/h x 6 h
or GFR ↓ > 25%
INJURY
↑ sCr x 2.0
<5 ml/Kg/h x 126 h
or GFR ↓ > 50%
FAILURE
↑ sCr x 3.0
< 3 ml/Kg/h for 24 h
or GFR ↓ > 75%
or anuria x 12 h
or sCr ≥ 4 mg/dL
or absolute ↑ sCr ≥ 0.5 mmg/dL
LOSS
Dialysis dependence > 4 wks.
-
ESRD
Dialysis dependence > 3 mos.
-
Relationship to Mortality of AKI Defined
by the RIFLE Criteria
Ricci Z et al. Kidney Int 2008; 73: 538-546
Acute Renal Failure is an Independent Risk Factor
for Mortality in Acutely Ill Patients
Probability of Survival
1
NO ARF
n = 1063
0.8
0.6
ARF
n = 348
0.4
0.2
0
0
10
20
30
ICU Stay (days)
De Mendonça A et al. Intensive Care Med 26 : 915-921, 2000.
ADQI
Acute Dialysis Quality Initiative Consensus Group
ADQI
Potential Clinical Consequences of Organ Edema in Critically Ill Patients
Prowle et al, Nature Revs Nephrol 2009
Effect of Fluid Balance on Mortality in AKI
Bouchard J et al. Kidney Int 2009: 76:422-7
Fluid Balance: CRRT vs. IHD
IHD
CVVHD
Augustine JJ et al. AJKD 2004; 44: 1000-7
Hemodynamic Stability: CRRT vs. IHD
Augustine JJ et al. AJKD 2004; 44: 1000-7
Fluid Management in Shock
Observational studies from the CV surgical population
establish an association between severe fluid overload
and increased morbidity and mortality
In septic conditions and acute lung injury, both
observational and prospective studies suggest fluid
balance is an independent determinant of outcomes
%FO is a newly introduced clinical parameter for the
assessment of fluid overload in AKI patients
• The PICARD study strongly indicates correction of fluid
overload with CRRT is superior to that achieved with
conventional HD in critically ill AKI patients
Reperfusion in Cardiogenic Shock Complicating AMI
Cardiogenic Shock
Delayed onset shock Echo
to evaluate mechanical
defects
Early shock diagnosed on
hospital presentation
Fibrinolytic therapy if all of the following are present:
90 mins. To PCI
< 3H post STEMI onset
No contraindications
Arrange prompt transfer to invasive procedure capable
center
Arrange rapid transfer to invasive
procedure capable center
IABP
Cardiac cath. and Coronary angiography
1-2 vessel CAD
Mod. 3 vessel CAD
Severe 3 vessel CAD
Left Main CAD
PCI IRA
PCI IRA
Immediate CABG
Staged
multivessel
PCI
Staged CABG
Hochman JS Circulation 2003; 107:2998
Survival in Patients Undergoing
Early Revascularization vs. Initial Medical Stabilization
Hochman JS et al. JAMA 2006; 295: 2511
ACC/AHA/ESC Guidelines for the Treatment of Cardiogenic Shock in AMI
Class I
IABP when CS is not quickly reversed by pharmacologic therapy
Intraarterial monitoring
Early revascularization with either PCI or CABG for pts. < 75 yo who
develop shock within 36 hours of MI and who are suitable for revasc. that
can be performed ≤ 18 h of shock
Among pts. With STEMI, fibrinolytic therapy in those not suitable for
revasc. and have no contraindication to fibrinolysis
Unless assessed by invasive testing, echo to evaluate for possible
mechanical complications
Class IIa
PA catheterization
Early revasc. with either PCI or CABG for selected patients ≥ 75 yo who
develop shock within 36 h of MI and who are suitable for revasc. that can
be performed within 18 h of shock
Antman EM et al. Circulation 2004; 110: 558
Importance of Blood Pressure on Clot Dissolution
Prewitt RM et al. JACC 1994; 23: 794
ACC/AHA Guidelines on IABP after AMI
Class I
Hypotension (SBP< 90mmHg or ≥ 30 mmHg below baseline MAP
unresponsive to other intervention
Low-CO state
Cardiogenic shock not quickly reversed with pharmacologic therapy as a
stabilizing measure for angiography and prompt revascularization
Recurrent ischemic-type chest discomfort and hemodynamic instability,
poor LV function, or a large area of myocardium at risk
Class IIa
Refractory polymorphic VT
Class IIb
Refractory pulmonary congestion
Antman EM et al. Circulation 2004; 110: 588
Acute Inferior and RV MI
Differences between LV and RV MI
Clinical Features
LV MI
RV MI
Pulmonary congestion
Clear lung fields
S3 and S4
Right sided S3
New MR
New TR
Hypotension with distended neck
veins
Electrocardiogram
ST elevation in standard leads
ST elevation in V4R
Commonly associated with IWMI
Frequent A-V block
Hemodynamics
↑ PAWP
RAP ≥ 10 mmHg
RAP: PAWP ≥ 0.8
Specific Management
Fluid restriction
Fluid resuscitation
Preload and afterload reduction
Avoid preload reduction
Reperfusion therapy
Reperfusion therapy
Inotropes, if necessary
Inotropes, if necessary
Effect of Successful PCI
on RV Wall Motion after Acute RV MI
Bowers TR et al. NEJM 1998; 338: 933
ACC/AHA/ESC Guidelines for the Management of RV MI
Class I
Patients with IWMI with ST elevation and hemodynamic compromise
should be screened for RV MI by right precordial V4R lead to detect
ST elevation and by echocardiography
Among patients with ST elevation MI and RV MI
Early reperfusion, if possible
Atrioventricular synchrony should be attained and bradycardia corrected
RV preload should be optimized (initial volume challenge if pt. is
hemodyanamically unstable and JVP low)
RV afterload should be optimized, which usually requires treatment of
concurrent LV dysfunction
Inotropic support if hemodynamic instability does not respond to volume
challenge
Class IIa
If there is clinically significant RV dysfunction, delaying CABG for 4 wks to
allow time for recovery of contractile function, which occurs in most pts.
over a period of weeks to months
Antman EM et al.
Papillary Muscle Rupture After MI
Edwards WD Internal Med. 1994; pp 169-89
Early Surgery and
Native Valve Endocarditis Mortality
Lalani T et al. Circulation 2010; 121: 1005
Pulsus Alternans Vs. Paradoxus
Topol ET et al 2006
Electrical Alternans
Pericardial Effusion by CXR
Subcostal View of IVC During
Cardiac Tamponade
Spectrum of Presentations of Myocarditis
Excessive fatigue
Chest pain
Unexplained sinus tachycardia
Acute pericarditis
S3, S4, or summation gallop
Abnormal ECG
Abnormal echo
New cardiomegaly on CXR
Atrial or ventricular arrhythmias
Partial or complete heart block
New onset HF
Atypical MI
Cardiogenic shock
Sudden, unexpected death
Acute Diffuse Myocarditis
Outcomes of Fulminant Myocarditis
McCarthy RE et al. N Engl J Med 2000;342:690-695.
Role of Endomyocardial Biopsy in Various Clinical Scenarios
Clinical Scenario
Recomm. Class
LOE
1
New onset HF < 2 weeks duration associated with normal size or
dilated LV and hemodynamic compromise
I
B
2
New onset HF 2-3 mos. duration associated with dilated LV, and new ventricular
arrhythmias, 2nd or 3rd heart block or failure to respond to usual care within 1-2
wks
I
B
3
HF > 3 mos duration associated with a dilated LV and new ventricular arrhythmias
2nd or 3rd heart block or failure to respond to usual care within 1-2 wks
IIa
C
4
HF associated with DCM of any duration associated with suspected allergic
reaction and/or eosinophilia
IIa
C
5
HF associated with suspected anthracycline CM
IIa
C
6
HF associated with unexplained restrictive CM
IIa
C
7
Suspected cardiac tumors
IIa
C
8
Unexplained CM in children
IIa
C
9
New onset HF 2-3 mos. duration associated with dilated LV, without new
ventricular arrhythmias, 2nd or 3rd heart block and that responds to usual care
within 1-2 wks
IIb
B
10
HF > 3 mos duration associated with a dilated LV without new ventricular
arrhythmias 2nd or 3rd heart block and that responds to usual care within 1-2 wks
IIb
C
11
HF associated with unexplained HCM
IIb
C
12
Suspected ARVD
IIb
C
13
Unexplained ventricular arrhythmias
IIb
C
14
Unaexplained AF
III
C
Cooper LT et al. Circulation 2007; 116: 2216
ECMO Circuit Using a Roller Pump
Indications and Contraindications for
Initiation of ECMOa
Indication
Contraindication
Murray Scoreb ≥ 3
Irreversible cardiac or pulmonary disease
Severe Hypercapnea with pH < 7.20,
Pao2:Fio2 < 50-100 mmHg
Age > 65 years
Alveolar-arterial oxygen gradient > 600
mmHg without cardiogenic pulmonary
edema
Metastatic malignancy
Transpulmonary shunt >30%
Significant brain injury
Mechanical ventilation > 5-10 days
Multitrauma with high risk of bleeding
a. Criteria used to enroll patients in recent prospective studies
b. Measure of acute lung injury taking into account the Pao2:Fio2, extent of infiltration
on CXR, applied PEEP, and pulmonary compliance
Evidence-Based Approach to ECMO
Cardiogenic Shock:
In 85 studies done in 1996-2005:
50% survival when ECMO was initiated for cardiogenic shock, 44% survival if ECMO was
initiated following cardiac arrest (Nichol G et al. Resuscitation 2006; 70:381-94)
Postcardiotomy Cardiogenic Shock:
PCCS incidence is 3%-5%
1% of these pts. cannot be weaned from CPB and ECMO becomes only alternative to
enable support withdrawal
Survival ranges between 19% and 67%
In 219 PCCS pts. who received ECMO (Doll N et el. Ann Thorac Surg 2004; 77: 151-7)
30 day survival was 24%
62% required reoperation for bleeding
58% developed renal failure
13% LE ischemia
In 82 PCCS pts. Who received ECMO ( Ko WJ et al. Ann Thoarc Surg 2002; 73: 538-45)
45% were weaned
54% of these survived
47% of weaned required reoperation for bleeding
Fulminant Myocarditis:
Survival rates with ECMO 71%-83% (Kawahito K et al. AJC 1998; 82: 910-11)
But… in one study survival 93% without ECMO! (McCarthy RE et al.NEJM 2000;342:690-5)
Evidence-Based Approach to ECMO
Bridge to Transplant
Of 28 pts. with ECMO, 14 died before HT, 11 underwent HT, 3 recovered
without HT (Hoefer D et al. Ann Thorac Surg 2006; 82: 28-33)
Of 33 pts. with ECMO, 10 survived to VAD placement (6 survived to HT
with 1 y survival of 80%), 1 HT, 5 weaned off ECMO, 16 died on ECMO
(Pagani F e al. Ann Thorac Surg 2001; 71(suppl 3): S77-S81)
Early graft Failure after HT
In one series 10/11 weaned off ECMO ( Arpesella G et al. Transplant Proc. 2008; 36:
1404-11)
In another series 9/14 weaned off ECMO and 7/9 long term survivors
(Leprince P et al. Transplant Proc 2005; 37: 2879-80)
Factors Associated with Mortality in ECMO Users
Variables
OR
95% CI
P value
Model I: Pre ECMO factors
Diagnostic Groups
0.05
Non cardiac diagnosis
1
Ref. group
AMI
0.91
(0.37-2.22)
0.83
CM
0.88
(0.31-2.48)
0.81
Acute Myocarditis
0.18
(0.05-0.69)
0.01
Acute PE
0.32
(0.08-1.32)
0.11
Other Cardiac Diseases
1.88
(0.44-7.88)
0.39
Pao2 (mmHg)
0.04
≥ 149
1
Ref. Group
70-<149
2.34
(0.96-5.74)
0.06
< 70
2.70
(1.21-6.07)
0.02
0.42
(0.21-0.87)
0.02
Need for Dialysis
2.41
(1.34-4.34)
0.003
ECMO Duration (h)
1.0
(1.0-1.002)
0.86
Percutaneous Cannulation Technique
Model II: ECMO Complications
Thiagarajan RR et al. Ann Thorac Surg 2009; 87: 778-85
Conclusions-Cardiogenic Shock
CS can result from multiple etiologies, including AMI, cardiomyopathies
and acute myocarditis
The ultimate goal of hemodynamic therapy for CS is to restore
effective tissue perfusion and normalize cellular metabolism
The key consideration for pharmacological therapy in CS is which
agent(s) best address the physiological abnormalities of a given
clinical context
CS is frequently associated with AKI. While fluid resuscitation is a
therapeutic priority in CS complicated by AKI, severe fluid overload is
associated with increased morbidity and mortality
In CS complicating AMI, early circulatory support and early
revascularization are the essential tools to improve outcomes
If acute myocarditis is the suspected cause of CS, immediate
histological confirmation and mechanical circulatory support can be
life-saving