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5.2 Dr.yusuf Assegaf SpJP - Syok Kardiogenik

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  • 8/11/2019 5.2 Dr.yusuf Assegaf SpJP - Syok Kardiogenik

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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