5.2 dr.yusuf assegaf spjp - syok kardiogenik
TRANSCRIPT
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CARDIOGENIC SHOCK
Department of Cardiology and Vascular Medicine
Airlangga School of Medicine - Dr. Soetomo Teaching Hospital Surabaya
Mochamad Yusuf, MD FIHARika Yenni P, MD
Rommy, MD
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BACKGROUND
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BACKGROUND
Some facts:
The incidence remained stable
over the past 3 decades
In-hospital mortality: 60%
(SHOCK Trial Registry) and
50-80% (older series)
Mostly after reaching hospital
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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
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CIRCULATORY SHOCK
Normal chamber & usuallypreserved contractility
Distributive Shock Cardiogenic Shock
Large ventricle & poorcontractility
In tamponade: pericardial effusion,
small RV & LV, dilated IVC; inpulmonary embolism or
pneumothorax: dilated RV, small LV
Obstructive Shock
Small chamber & normal/
high contractility
Hypovolemic Shock
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Brain: Altered mental status
Kidney: Oliguria
Skin: Mottled, clammy
Tachycardia
Blood lactate !
CIRCULATORY SHOCK
Arterial hypotension
Present
Circulatory
shock
Est. CO or SVO2
Normalor high
Low
LowCVP
HighCVP
Distributiveshock
Hypovolemicshock
Cardiogenic& obstructive
shock
Shock: clinical expression of circulatory failure
that results in inadequate cellular oxygenutilization. Vincent JL, 2013
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Cardiogenic Shock
Large ventricle & poorcontractility
CARDIOGENIC SHOCK
Persistent hypotension and tissue hypoperfusion
due to cardiac dysfunction with adequate
intravascular volumeand LV filling pressure.
Hypotension, tachycardia, oliguria, cool extremities & altered mental status
Sustained hypotension: SBP < 90 mm Hg for 30 mins
Low cardiac index: 15 mmHg
Clinical Sign
Hemodynamic Finding
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ETIOLOGY
LV Failure78%
MR7%
VSR4%
RV infarct3%
Tamponade / Free wall rupture1%
Others7%
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 filling (MS / LAmyxoma)
Acute mitral / aortic regurgitation(chordal rupture)
TamponadeNon Cardiac:
Severe pulmonary arterialhypertension
Acute severe pulmonary embolism
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PATHOPHYSIOLOGY
Acute MI
LVEDP !Lung Edema
Hypoxia
Cardiac Output "Stroke Volume "
Hypotension
Coronary
perfusion "Peripheral
perfusion "
VasoconstrictionFluid retention
SVR "Pro-inflammationCathecolamin sensitivity"Contractility "
NO !Peroxynitrite !
IL-6 !TNF-#!
eNOS iNOS
Inotropes /
Vasopressors x
Mechanical supports:IABP/LVADx
Reperfusions:PCI/CABG
x
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MYOCARDIAL ISCHEMIA
Cell
death
No return
of function
Reperfusion
Significantresidual stenosis
Myocardial
stunning
Both stunning& hibernation
Myocardial
hibernating
Innotropic
support
Relief ofischemia
Return of
function
Hollenberg, 1999
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ESC ALGORITHM
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MECHANICAL SUPPORT
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IATROGENIC SHOCK
Coronary occlusion
LV compliance " PCWP ! CO "or unchanged
Redistribution of
intravascular volumeto lung
Pulmonary edema
Lower CO
Hypotension
Cardiogenic shock
RV infarction
RV RVEDP !(>15)
CVP !
Shift of interventricularseptum toward LV
Impaired LV filling &systolic function due tochanges in LV geometry
Low SV Compensatory
tachycardia
DiureticPreload "
Intravascular volume "
SVR "
$blocker
Reynolds, 2008
ACEiNitrate
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ASSESSMENT OF CARDIOGENIC SHOCK
Systemic hypotension(SBP
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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-RayNew or worsening pulmonary congestion
Echocardiographic
Hemodynamic assessment/monitoring (left/right ventricular systolicfunction, decreased stroke volume, cardiac output/index, diastolic function,PCWP, PA pressure, SVR, PVR, IVC)
Contractility Mechanical abnormalities (ventricular septal/free wall rupture, pericardial
fluid with tamponade)
Valvular dysfunction (severe mitral regurgitation)
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INITIAL MANAGEMENT
E
M
0min
R
G
E
N
5
min IC
C
Y
R
15min
CU
O
M 60min
EARLY TRIAGE & MONITORING
INITIAL RESUSCITATION
Age: 6574, %75 Heart rate >100 beats/ min Systolic BP20/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 interventioncenter when signs and/or symptoms of ongoing myocardial
ischemia (e.g. STEMI)
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INITIAL MANAGEMENT
Start high flow O2
Establish i.v. access
CORRECT: hypoglycemia & hypocalcemia
TREAT: sustaned arrhythmias: brady or tachy, Isotonic saline-fluid 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
0min
R
G
E
N
5
min IC
C
Y
R
15min
CU
O
M 60min
EARLY TRIAGE & MONITORING
INITIAL RESUSCITATION
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INITIAL MANAGEMENT
Central venous saturation
(ScvO2) %70% (provided SpO2
%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
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Take Home Messages
Cardiogenic shock is the most common cause ofdeath in patients hospitalized with acute myocardial
infarction and is associated with a poor prognosis.
Appropriate treatmentis based on a good
understanding of the underlying pathophysiological
mechanisms.
Cardiogenic Shock is a treatable illness with a
reasonable chance for full recovery.
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THANK YOU
Cardiogenic Shock
Mochamad Yusuf
2013
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VASOPRESSORS AND INOTROPES
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ESC ALGORITHM
ESC 2012
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TAKE HOME MESSAGE
KNOW YOUR ENEMY
TREAT UNDERLYING DISEASE
SUPPORT HEMODYNAMICS
BE FAST
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LEFT VENTRICULAR ASSIST DEVICES (LVAD)
MECHANICAL SUPPORT
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MECHANICAL SUPPORT
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MECHANICAL SUPPORT
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MECHANICAL SUPPORT
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INITIAL MANAGEMENT
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IABP-SHOCK Trial
MECHANICAL SUPPORT
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MECHANICAL SUPPORT
IABP-SHOCK Trial II