CARDIOGENIC SHOCK
Mochamad Yusuf, MD FIHA Rika Yenni P, MD Rommy, MD Department of Cardiology and Vascular Medicine Airlangga School of Medicine - Dr. Soetomo Teaching Hospital Surabaya
BACKGROUND
BACKGROUND Some facts: The incidence remained stable over the past 3 decades In-hospital mor tality: 60% (SHOCK Trial Registry) and 50-80% (older series) Mostly after reaching hospital
CIRCULATORY SHOCK Arterial hypotension Brain: Altered mental status Tachycardia
Absent Kidney: Oliguria
Chronic hypotension? Syncope (if transient)
Skin: Mottled, clammy Blood lactate ↑
Vincent JL, 2013
Distributive Shock
CIRCULATORY SHOCK
Cardiogenic Shock
Obstructive 2%
Normal chamber & usually preserved contractility
Hypovolemic Shock
Hypovolemic 16% Distributive septic 62%
Large ventricle & poor contractility
Obstructive Shock
Cardiogenic 16%
Distributive non-septic 4% Small chamber & normal/ high contractility
In tamponade: pericardial effusion, small RV & LV, dilated IVC; in pulmonary embolism or pneumothorax: dilated RV, small LV
CIRCULATORY SHOCK Arterial hypotension Brain: Altered mental status
Present Tachycardia
Circulatory shock
Kidney: Oliguria
Est. CO or SVO2
Skin: Mottled, clammy
Low
Normal or high
Blood lactate ↑
Shock: clinical expression of circulatory failure that results in inadequate cellular oxygen utilization.
Distributive shock
Low CVP
Hypovolemic shock Vincent JL, 2013
High CVP
Cardiogenic & obstructive shock
CARDIOGENIC SHOCK Cardiogenic Shock
Persistent hypotension and tissue hypoperfusion due to cardiac dysfunction with adequate intravascular volume and LV filling pressure.
Clinical Sign
Large ventricle & poor contractility
Hypotension, tachycardia, oliguria, cool extremities & altered mental status
Hemodynamic Finding • 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
ETIOLOGY Cardiac: • Acute myocardial infarction • End-stage cardiomyopathy • Myocarditis • LVOT obstruction (AS / HOCM) • Obstruction to LV filling (MS / LA myxoma) • Acute mitral / aortic regurgitation (chordal rupture) • Tamponade Non Cardiac: • Severe pulmonary arterial hypertension • Acute severe pulmonary embolism
Causes of Cardiogenic shock in AMI (SHOCK trial) Others 7% Tamponade / Free wall rupture 1% RV infarct 3% VSR 4%
LV Failure 78%
MR 7% Topalian, 2008
PATHOPHYSIOLOGY Acute MI LV Dysfunction
SIRS Cardiac Output ↓ Stroke Volume ↓
•eNOS • iNOS
Inotropes / Vasopressors
x
Peripheral perfusion ↓
•NO ↑ •Peroxynitrite ↑ •IL-6 ↑ •TNF-α ↑
Diastolic
Mechanical supports: IABP/LVAD Hypotension
LVEDP ↑ Lung Edema
Coronary perfusion ↓
Hypoxia
Ischemia
x Reperfusions: PCI/CABG
Vasoconstriction Fluid retention
•SVR ↓ •Pro-inflammation •Cathecolamin sensitivity↓ •Contractility ↓
x
Systolic
Progresive LV Dysfunction
Death
MYOCARDIAL ISCHEMIA Hollenberg, 1999
No return of function
Cell death
Significant residual stenosis
Reperfusion
Myocardial hibernating Both stunning & hibernation Myocardial stunning
Relief of ischemia Innotropic support
Return of function
ESC ALGORITHM
Indications for implementation of IABP and LVAD In selected patients with myocardial infarction (STEMI) INDIKASI!
GUIDELINE! ESC
IABP! Complicated by cardiogenic shock! Treatment with PCI!
ACC/AHA German/Austrian
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Treatment with fibrinolysis/with no
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perfusion strategy! Before transport to an interventional centre $ for PCI!
LVAD!
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MECHANICAL SUPPORT
IATROGENIC SHOCK Coronary occlusion
• •
Low SV Compensatory tachycardia
• • •
LV compliance ↓ PCWP ↑ CO ↓ or unchanged Redistribution of intravascular volume to lung Pulmonary edema
Diuretic
• •
RV RVEDP ↑ (>15) CVP ↑
Shift of interventricular septum toward LV
Preload ↓ Intravascular volume ↓
β blocker ACEi Nitrate
RV infarction
Lower CO SVR ↓
Impaired LV filling & systolic function due to changes in LV geometry
Hypotension Cardiogenic shock
Reynolds, 2008
ASSESSMENT OF CARDIOGENIC SHOCK Jugular venous distention, crackles in the lungs & peripheral edema Systemic hypotension (SBP <90 mm Hg or ↓MAP by 30 mm Hg)
Low pulse pressure & usually tachycardia
Heart sounds usually distant, & may be present S3&S4
Signs of hypoperfusion: altered mental status & ↓urine output
Ashen/cyanotic and cool skin; mottled extremities
Rapid & faint peripheral pulses and may be irregular (if arrhythmias)
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 fluid with tamponade) • Valvular dysfunction (severe mitral regurgitation)
INITIAL MANAGEMENT EARLY TRIAGE & MONITORING
E M E R G E N C Y R O O M
0 min
5 min
15 min
60 min
I C C U
Age: 65–74, ≥75 • Heart rate >100 beats/ min • Systolic BP<100 mmHg • Proportional pulse pressure ≤25 mmHg (CI <2.2 L/min/m2) • Orthopnea (PCWP >22 mmHg) • Tachypnea (>20/min), (>30/min) • Killip class II-IV • Clinical symptoms of tissue hypoperfusion/hypoxia
INITIAL RESUSCITATION
• • •
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 EARLY TRIAGE & MONITORING
E M E R G E N C Y R O O M
0 min
Start high flow O2 Establish i.v. access 5 min
15 min
60 min
I C C U
INITIAL RESUSCITATION 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)
INITIAL MANAGEMENT CVP 8-12 mmHg PCWP ≤ 18 mmHg or below C e n t r a l ve n o u s s a t u r a t i o n (ScvO2) ≥70% (provided SpO2 ≥93% and Hb level ≥9 g/dL) MAP ≥ 60 mmHg Urinary ouput ≥ 0,5 ml/hr/kgBW Arterial pH of 7.3-7.5
In persistent drug-resistant cardiogenic shock, consider mechanical circulatory support
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
MECHANICAL SUPPORT LEFT VENTRICULAR ASSIST DEVICES (LVAD)
MECHANICAL SUPPORT
MECHANICAL SUPPORT
MECHANICAL SUPPORT
INITIAL MANAGEMENT
MECHANICAL SUPPORT IABP-SHOCK Trial
MECHANICAL SUPPORT IABP-SHOCK Trial II