CARDIOGENIC SHOCK

Department of Cardiology and Vascular Medicine

Airlangga School of Medicine - Dr. Soetomo Teaching Hospital Surabaya
Mochamad Yusuf, MD FIHA
Rika Yenni P, MD
Rommy, MD
BACKGROUND
BACKGROUND
Some facts:
The incidence remained stable
over the past 3 decades
I n-hospi tal mortal i ty: 60%
(SHOCK Trial Registry) and
50-80% (older series)
Mostly after reaching hospital
Brain: Altered mental status
CIRCULATORY SHOCK
Kidney: Oliguria
Skin: Mottled, clammy
Tachycardia
Blood lactate !
Arterial hypotension
Absent
Chronic
hypotension?
Syncope (if
transient)
Vincent JL, 2013
CIRCULATORY SHOCK
Distributive non-septic
4%
Cardiogenic
16%
Hypovolemic
16%
Obstructive
2%
Distributive septic
62%
Normal chamber & usually
preserved contractility
Distributive Shock Cardiogenic Shock
Large ventricle & poor
contractility
In tamponade: pericardial effusion,
small RV & LV, dilated IVC; in
pulmonary embolism or
pneumothorax: dilated RV, small LV
Obstructive Shock
Small chamber & normal/
high contractility
Hypovolemic Shock
Brain: Altered mental status
Kidney: Oliguria
Skin: Mottled, clammy
Tachycardia
Blood lactate !
CIRCULATORY SHOCK
Arterial hypotension
Present
Circulatory
shock
Est. CO or S
VO2
Normal
or high
Low
Low
CVP
High
CVP
Distributive
shock
Hypovolemic
shock
Cardiogenic
& obstructive
shock
Shock: clinical expression of circulatory failure
that results in inadequate cellular oxygen
utilization.
Vincent JL, 2013
Cardiogenic Shock
Large ventricle & poor
contractility
CARDIOGENIC SHOCK
Persistent hypotension and tissue hypoperfusion
due to cardiac dysfunction with adequate
intravascular volume and LV lling pressure.
Hypotension, tachycardia, oliguria, cool extremities & altered mental status

Sustained hypotension: SBP < 90 mm Hg for 30 mins

Low cardiac index: <1.8 L/min/m2 (supported) or 2.0

-2.2 L/min/m2 (unsupported)

Elevated PCWP: >15 mmHg

Clinical Sign

Hemodynamic Finding
ETIOLOGY
LV Failure
78%
MR
7%
VSR
4%
RV infarct
3%
Tamponade / Free wall rupture
1%
Others
7%
Causes of Cardiogenic shock in AMI
(SHOCK trial)
Topalian, 2008
Cardiac:

Acute myocardial infarction

End-stage cardiomyopathy

Myocarditis

LVOT obstruction (AS / HOCM)

Obstruction to LV lling (MS / LA

myxoma)

Acute mitral / aortic regurgitation

(chordal rupture)

Tamponade
Non Cardiac:

Severe pulmonary arterial

hypertension

Acute severe pulmonary embolism

PATHOPHYSIOLOGY
Acute MI
LV Dysfunction
Systolic Diastolic
Ischemia
Progresive
LV Dysfunction
Death
LVEDP !
Lung Edema
Hypoxia
Cardiac Output "
Stroke Volume "
Hypotension
Coronary
perfusion "
Peripheral
perfusion "
Vasoconstriction
Fluid retention
SIRS
SVR "

Pro-inammation
Cathecolamin sensitivity"
Contractility "
NO !
Peroxynitrite !
IL-6 !
TNF-# !

eNOS

iNOS
Inotropes /
Vasopressors
x
Mechanical supports:
IABP/LVAD
x
Reperfusions:
PCI/CABG
x
MYOCARDIAL ISCHEMIA
Cell
death
No return
of function
Reperfusion
Signicant
residual stenosis
Myocardial
stunning
Both stunning
& hibernation
Myocardial
hibernating
Innotropic
support
Relief of
ischemia
Return of
function
Hollenberg, 1999
ESC ALGORITHM
Indications for implementation of IABP and LVAD
In selected patients with myocardial infarction
(STEMI)
INDIKASI GUIDELINE
IABP
ESC
!"#!
ACC/AHA
!"#%
German/Austrian
!"#!
Complicated by cardiogenic shock IIb IIa
Treatment with PCI !
Treatment wi th fi bri nol ysi s/ wi th no
perfusion strategy
"
Before transport to an interventional centre
for PCI
"
LVAD
IIb IIb
27
! : dapat dipertimbangkan namun bukti masih belum jelas; ": direkomendasikan
MECHANICAL SUPPORT
IATROGENIC SHOCK
Coronary occlusion
LV compliance "
PCWP !
CO " or unchanged
Redistribution of
intravascular volume
to lung
Pulmonary edema
Lower CO
Hypotension
Cardiogenic shock
RV infarction
RV RVEDP ! (>15)
CVP !
Shift of interventricular
septum toward LV
Impaired LV lling &
systolic function due to
changes in LV geometry

Low SV

Compensatory
tachycardia
Diuretic
Preload "
Intravascular volume "
SVR "
$ blocker
Reynolds, 2008
ACEi
Nitrate
ASSESSMENT OF CARDIOGENIC SHOCK
Systemic hypotension
(SBP <90 mm Hg or
!MAP by 30 mm Hg)
Ashen/cyanotic and cool
skin; mottled extremities
Rapid & faint peripheral
pulses and may be
irregular (if arrhythmias)
Jugular venous
distention, crackles in
the lungs & peripheral
edema
Heart sounds usually
distant, & may be present
S
3
&S
4
Low pulse pressure &
usually tachycardia
Signs of hypoperfusion:
altered mental status &
!urine output
ASSESSMENT OF CARDIOGENIC SHOCK
Laboratory

Elevated lactate level and decreased serum bicarbonate

Increasing blood urea nitrogen and creatinine

Electrocardiographic
New or recurrent electrocardiographic evidence of ischemia or infarction
Chest X-Ray
New or worsening pulmonary congestion
Echocardiographic

Hemodynamic assessment/monitoring (left/right ventricular systolic

function, decreased stroke volume, cardiac output/index, diastolic function,
PCWP, PA pressure, SVR, PVR, IVC)

Contractility

Mechanical abnormalities (ventricular septal/free wall rupture, pericardial

uid with tamponade)

Valvular dysfunction (severe mitral regurgitation)

INITIAL MANAGEMENT
E
M
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G
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N
C
Y
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0
min
I
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5
min
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15
min
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60
min
I
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C
U
EARLY TRIAGE & MONITORING
INITIAL RESUSCITATION
Age: 6574, %75

Heart rate >100 beats/ min

Systolic BP<100 mmHg

Proportional pulse pressure &25 mmHg (CI <2.2 L/min/m

2
)

Orthopnea (PCWP >22 mmHg)

Tachypnea (>20/min), (>30/min)

Killip class II-IV

Clinical symptoms of tissue hypoperfusion/hypoxia

Arterial line and CVC

Standard transthoracic echocardiogram (assess LV&RV

function and mechanical complications of MI)

Early coronary angiography in myocardial intervention

center when signs and/or symptoms of ongoing myocardial
ischemia (e.g. STEMI)
INITIAL MANAGEMENT
Start high ow O2
Establish i.v. access
CORRECT: hypoglycemia & hypocalcemia
TREAT: sustaned arrhythmias: brady or tachy, Isotonic saline-uid challenge of 20-30
ml/kg/BW over a 30 until CVP 8-12 mmHg or perfusion improves (max500 ml)
CONSIDER: NIV mechanical ventilation for comfort (fatigue, distress) or to correct
acidosis/ hypoxemia
INOTROPIC SUPPORT (dobutamine and/or vasopressor support)
E
M
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G
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N
C
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0
min
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C
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5
min
I
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15
min
I
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C
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60
min
I
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C
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EARLY TRIAGE & MONITORING
INITIAL RESUSCITATION
INITIAL MANAGEMENT
Cent ral venous sat urat i on
(ScvO
2
) %70% (provided SpO
2

%93% and Hb level %9 g/dL)
In persistent drug-resistant cardiogenic shock,
consider mechanical circulatory support
MAP % 60 mmHg
PCWP & 18 mmHg or below
CVP 8-12 mmHg
Urinary ouput % 0,5 ml/hr/kgBW
Arterial pH of 7.3-7.5
Take Home Messages
Cardiogenic shock is the most common cause of
death in patients hospitalized with acute myocardial
infarction and is associated with a poor prognosis.
Appropriate treatment is based on a good
understanding of the underlying pathophysiological
mechanisms.
Cardiogenic Shock is a treatable illness with a
reasonable chance for full recovery.
THANK YOU
Cardiogenic Shock
Mochamad Yusuf
2013
VASOPRESSORS AND INOTROPES
ESC ALGORITHM
ESC 2012
TAKE HOME MESSAGE
KNOW YOUR ENEMY
TREAT UNDERLYING DISEASE
SUPPORT HEMODYNAMICS
BE FAST
LEFT VENTRICULAR ASSIST DEVICES (LVAD)
MECHANICAL SUPPORT
MECHANICAL SUPPORT
MECHANICAL SUPPORT
MECHANICAL SUPPORT
INITIAL MANAGEMENT
IABP-SHOCK Trial
MECHANICAL SUPPORT
MECHANICAL SUPPORT
IABP-SHOCK Trial II