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Cardiogenic shock
Core Review
2020.12.02
CCM F. 김하영
Definition
 Serious condition that occurs when heart cannot pump enough
blood and oxygen to the brain, kidneys, and other vital organs.
 low cardiac output, end-organ hypoperfusion and hypoxia
 Hypotension refractory to volume resuscitation
end-organ hypoperfusion requiring pharmacological or mechanical
intervention
 AMI with LV dysfunction is the most frequent cause
 In-hospital mortality high(27-51%)
Definition
 Clinical features of cardiogenic shock as defined in Contemporary
Trials and Guidelines
Clinical
definition
SHOCK Trial
(1999)
IABP-SOAP II
(2012)
EHS-PCI
(2012)
ESC-HF
Guidelines(2016)
KAMIR-NIH
(2018)
• Cardiac
disorder that
results in both
clinical and
biochemical
evidence of
tissue hypo-
perfusion
• SBP <90 mm Hg
for >30 min or
vasopressor support to
maintain SBP >90 mm
Hg
• Evidence of end-organ
damage (UO <30 mL/h
or cool extremities)
• Hemodynamic criteria:
CI <2.2 and PCWP >15
mm Hg
• MAP <70 mm Hg
or SBP <100 mm Hg
despite adequate
fluid resuscitation
(at least 1 L of
crystalloids or 500
mL of colloids)
• Evidence of end-
organ damage (AMS,
mottled skin, UO
<0.5 mL/kg for 1 h,
or serum lactate >2
mmol/L)
• SBP <90 mm
Hg for 30 min or
inotropes use to
maintain SBP >90
mm Hg
• Evidence of
end-organ
damage and
increased filling
pressures
• SBP <90 mm Hg
with appropriate
fluid resuscitation
with clinical and
laboratory evidence
of end-organ
damage
• Clinical: cold
extremities, oliguria,
AMS, narrow pulse
pressure.
• Laboratory:
metabolic acidosis,
elevated serum
lactate, elevated
serum creatinine
• SBP <90 mm Hg
for >30 min or
supportive
intervention to
maintain SBP >90
mm Hg
• Evidence of end-
organ damage
(AMS, UO <30
mL/h, or cool
extremities)
JAHA 2019;119.011991
Epidemiology
Jones TL, et al. Open Heart 2019;6:e000960
 AMI with LV failure 60-80% of
cardiogenic shock(CS).
 Higher incidences of CS are observed
in women, Asian/Pacific Islanders, and
patients >75 years.
 Survivors of MI‐associated CS have an
18.6% risk of 30‐day readmission after
discharge, with a median time of
10 days.
Epidemiology
 The initial cardiac insult may stem
from various etiologies
- AMI-CS is typically associated with >40%
loss of left ventricular (LV) myocardium
- Mechanical complications may also
precipitate AMI-CS
- CS may additionally occur in patients
with heart failure
- Post-cardiotomy CS complicates 0.1% to
0.5% of cardiac surgeries
JACC: heart failure.2020:879-91
Pathophysiology
Circulation. 2017;136:e232–e268
European Journal of Heart Failure (2020) 22, 1315–1341
 In the setting of CS, classic ACS symptoms and signs are combined
with altered mental status, hypotension, arrhythmia, diminished
pulses, dyspnea, peripheral edema, jugular venous distention, and
orthopnea
Clinical presentation and physical examination
 Cool extremities and signs of pul. Congestion: cold & wet
 Euvolemic(previous MI or CKD): dry & cold
 Systemic inflammatory response system or sepsis with MI: wet &warm
Clinical presentation and physical examination
Cardiogenic shock classification
Catheter Cardiovasc Interv. 2019;94:29–37
• Society for Cardiovascular Angiography and Interventions(SCAI) clinical expert
consensus statement on the classification of cardiogenic shock
• The(A) modifier is applied to describe patients who have had a cardiac arrest
irrespective of duration.
Cardiogenic shock classification
Laboratory evaluation
• ECG
- ST‐segment elevation, ST‐segment depression, and
non–ST‐segment deviation
• Complete blood counts and metabolic panels
• Cardiac enzymes
• NT‐proBNP
• ABGA
• Lactate
• Chest x-ray
• Echocardiography may be beneficial,
however, it should not delay cardiac catheterization
• CT scan (contrast)
Circulation. 2017;136:e232–e268
Laboratory evaluation
Circulation. 2017;136:e232–e268
European Journal of Heart Failure (2020) 22, 1315–1341
Stabilization and resuscitation strategy
European Journal of Heart Failure (2020) 22, 1315–1341
Heart Fail Rev (2020) 25:183–194
Stabilization and resuscitation strategy
• Intravenous fluids
 Echocardiography: assess right-sided heart volume status
and rule out pericardial fluid collection
 Hypovolemia: boluses of crystalloids (250–500 mL)
• Oxygenation and ventilation
 Continuous pulse oximetry monitoring
 Blood oxygen saturations of >90%
 Invasive ventilation: Low tidal volume strategy(5–7 mL/kg)
• Vasopressor support
 Mean arterial pressure goal of >65 mmHg
 The optimal first-line vasoactive medication in CS remains
unclear
 Pulmonary vasoactive agent: inodilators, phosphodiesterase
III inhibitors, or nitric oxide
Stabilization and resuscitation strategy
JAHA.2019.119.01199
Stabilization and resuscitation strategy
Stabilization and resuscitation strategy
Circulation. 2017;136:e232–e268
Stabilization and resuscitation strategy
• Continuous renal replacement therapy
 CRRT: stage 2 kidney injury as defined by elevated serum creatinine (≥2 x baseline) and urine output
<0.5 mL/ kg per hour for ≥12 hours
• Hemodynamic monitoring
 BP, arterial line, continuous pulse oximetry, temperature, respiratory rate, urinary output monitoring
 Mixed venous oxygen saturation (SvO2)
- measured from a sample of blood from the central venous system, ideally from the distal port of a
pulmonary artery catheter
- low SvO2: reduced CO, anemia, hypoxemia, or increased oxygen consumption
 Echocardiography and catheterization are used together to assess the hemodynamic response to
intervention
 Pulmonary artery catheter (PAC)
- precise measurements of fluid states, central venous oxygen saturation, response to therapy, and
indicates the effectiveness of ventricular support
Stabilization and resuscitation strategy
MCS(Mechanical circulatory support) devices
• In CS, end diastolic and systolic
volumes increase, stroke volume
decreases, and end systolic
pressure decreases reflecting the
overall reduction in LV contractility
and output.
• MCS devices alter hemodynamics
in an attempt to restore CO and
normalise perfusion pressures
• IABP(intra‐aortic balloon pump)
• Axial flow pumps(Impella)
• Left atrial-to-femoral arterial ventricular
assist devices(Tandem heart)
• ECMO(venous‐arterial extracorporeal
membrane oxygenation )
MCS devices(Mechanical circulatory support)
• IABP
 IABP decrease myocardial oxygen consumption, increase coronary artery
perfusion, decrease afterload and modestly increase cardiac output (0.8–1L/min)
 Patients with CS with post AMI mechanical complication
 It can be considered in select patients with profound CS when other MCS
devices are not available, are contraindicated, or cannot be placed
• ECMO
 Drainage of venous blood, passing it through an oxygenator and returning
the oxygenated blood to systemic circulation using a centrifugal pump
 Performed centrally by cannulation of the right atrium and aorta or peripherally with cannulation of
the femoral artery and vein
 V-A ECMO may be the preferred temporary MCS option when there is poor oxygenation that is not
expected to rapidly improve with an alternative temporary MCS device or during CPR
• Coronary angiography
 The most important investigation in
patients diagnosed with CS is coronary
angiography
 Identify the precise location of the lesion
that precipitated CS
• PCI strategy
 Coronary reperfusion is an essential
therapeutic intervention for patients with
ACS complicated by CS
• Heart transplantation
 Cardiac transplantation, particularly for
patients requiring biventricular MCS, often
represents the only hope for meaningful,
long-term recovery.
Stabilization and resuscitation strategy
• Critically ill patients are at risk of developing
complications such as ventilator-associated
pneumonia, delirium, ICU-acquired weakness,
central line–associated bloodstream infection,
stress ulcers, and venous thromboembolism
• These complications are associated with an
increased risk of morbidity, mortality, and length
of stay
Reference
 Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association.
Circulation. 2017;136:e232–e268
 Cardiogenic shock: evolving definitions and future directions in management. Open Heart 2019;6:e000960
 Cardiogenic Shock. JAHA.2019.119.01199
 Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance. Intensive Care Med (2016)
42:147–163
 Cardiogenic Shock Classification to Predict Mortality in the Cardiac Intensive Care Unit. JACC. 2019: 2117–28
 SCAI clinical expert consensus statement on the classification of cardiogenic shock. Catheter Cardiovasc Interv.
2019;94:29–37
 Management of Acute Heart Failure during an Early Phase. Int J Heart Fail. 2020 Apr;2(2):91-110
 Epidemiology, pathophysiology and contemporary management of cardiogenic shock. European Journal of
Heart Failure (2020) 22, 1315–1341

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20201202 cardiogenic shock

  • 2. Definition  Serious condition that occurs when heart cannot pump enough blood and oxygen to the brain, kidneys, and other vital organs.  low cardiac output, end-organ hypoperfusion and hypoxia  Hypotension refractory to volume resuscitation end-organ hypoperfusion requiring pharmacological or mechanical intervention  AMI with LV dysfunction is the most frequent cause  In-hospital mortality high(27-51%)
  • 3. Definition  Clinical features of cardiogenic shock as defined in Contemporary Trials and Guidelines Clinical definition SHOCK Trial (1999) IABP-SOAP II (2012) EHS-PCI (2012) ESC-HF Guidelines(2016) KAMIR-NIH (2018) • Cardiac disorder that results in both clinical and biochemical evidence of tissue hypo- perfusion • SBP <90 mm Hg for >30 min or vasopressor support to maintain SBP >90 mm Hg • Evidence of end-organ damage (UO <30 mL/h or cool extremities) • Hemodynamic criteria: CI <2.2 and PCWP >15 mm Hg • MAP <70 mm Hg or SBP <100 mm Hg despite adequate fluid resuscitation (at least 1 L of crystalloids or 500 mL of colloids) • Evidence of end- organ damage (AMS, mottled skin, UO <0.5 mL/kg for 1 h, or serum lactate >2 mmol/L) • SBP <90 mm Hg for 30 min or inotropes use to maintain SBP >90 mm Hg • Evidence of end-organ damage and increased filling pressures • SBP <90 mm Hg with appropriate fluid resuscitation with clinical and laboratory evidence of end-organ damage • Clinical: cold extremities, oliguria, AMS, narrow pulse pressure. • Laboratory: metabolic acidosis, elevated serum lactate, elevated serum creatinine • SBP <90 mm Hg for >30 min or supportive intervention to maintain SBP >90 mm Hg • Evidence of end- organ damage (AMS, UO <30 mL/h, or cool extremities) JAHA 2019;119.011991
  • 4. Epidemiology Jones TL, et al. Open Heart 2019;6:e000960  AMI with LV failure 60-80% of cardiogenic shock(CS).  Higher incidences of CS are observed in women, Asian/Pacific Islanders, and patients >75 years.  Survivors of MI‐associated CS have an 18.6% risk of 30‐day readmission after discharge, with a median time of 10 days.
  • 5. Epidemiology  The initial cardiac insult may stem from various etiologies - AMI-CS is typically associated with >40% loss of left ventricular (LV) myocardium - Mechanical complications may also precipitate AMI-CS - CS may additionally occur in patients with heart failure - Post-cardiotomy CS complicates 0.1% to 0.5% of cardiac surgeries JACC: heart failure.2020:879-91
  • 7.  In the setting of CS, classic ACS symptoms and signs are combined with altered mental status, hypotension, arrhythmia, diminished pulses, dyspnea, peripheral edema, jugular venous distention, and orthopnea Clinical presentation and physical examination
  • 8.  Cool extremities and signs of pul. Congestion: cold & wet  Euvolemic(previous MI or CKD): dry & cold  Systemic inflammatory response system or sepsis with MI: wet &warm Clinical presentation and physical examination
  • 9. Cardiogenic shock classification Catheter Cardiovasc Interv. 2019;94:29–37 • Society for Cardiovascular Angiography and Interventions(SCAI) clinical expert consensus statement on the classification of cardiogenic shock • The(A) modifier is applied to describe patients who have had a cardiac arrest irrespective of duration.
  • 11. Laboratory evaluation • ECG - ST‐segment elevation, ST‐segment depression, and non–ST‐segment deviation • Complete blood counts and metabolic panels • Cardiac enzymes • NT‐proBNP • ABGA • Lactate • Chest x-ray • Echocardiography may be beneficial, however, it should not delay cardiac catheterization • CT scan (contrast) Circulation. 2017;136:e232–e268
  • 12. Laboratory evaluation Circulation. 2017;136:e232–e268 European Journal of Heart Failure (2020) 22, 1315–1341
  • 13. Stabilization and resuscitation strategy European Journal of Heart Failure (2020) 22, 1315–1341
  • 14. Heart Fail Rev (2020) 25:183–194 Stabilization and resuscitation strategy • Intravenous fluids  Echocardiography: assess right-sided heart volume status and rule out pericardial fluid collection  Hypovolemia: boluses of crystalloids (250–500 mL) • Oxygenation and ventilation  Continuous pulse oximetry monitoring  Blood oxygen saturations of >90%  Invasive ventilation: Low tidal volume strategy(5–7 mL/kg) • Vasopressor support  Mean arterial pressure goal of >65 mmHg  The optimal first-line vasoactive medication in CS remains unclear  Pulmonary vasoactive agent: inodilators, phosphodiesterase III inhibitors, or nitric oxide
  • 15. Stabilization and resuscitation strategy JAHA.2019.119.01199
  • 17. Stabilization and resuscitation strategy Circulation. 2017;136:e232–e268
  • 18. Stabilization and resuscitation strategy • Continuous renal replacement therapy  CRRT: stage 2 kidney injury as defined by elevated serum creatinine (≥2 x baseline) and urine output <0.5 mL/ kg per hour for ≥12 hours • Hemodynamic monitoring  BP, arterial line, continuous pulse oximetry, temperature, respiratory rate, urinary output monitoring  Mixed venous oxygen saturation (SvO2) - measured from a sample of blood from the central venous system, ideally from the distal port of a pulmonary artery catheter - low SvO2: reduced CO, anemia, hypoxemia, or increased oxygen consumption  Echocardiography and catheterization are used together to assess the hemodynamic response to intervention  Pulmonary artery catheter (PAC) - precise measurements of fluid states, central venous oxygen saturation, response to therapy, and indicates the effectiveness of ventricular support
  • 20. MCS(Mechanical circulatory support) devices • In CS, end diastolic and systolic volumes increase, stroke volume decreases, and end systolic pressure decreases reflecting the overall reduction in LV contractility and output. • MCS devices alter hemodynamics in an attempt to restore CO and normalise perfusion pressures • IABP(intra‐aortic balloon pump) • Axial flow pumps(Impella) • Left atrial-to-femoral arterial ventricular assist devices(Tandem heart) • ECMO(venous‐arterial extracorporeal membrane oxygenation )
  • 21.
  • 22. MCS devices(Mechanical circulatory support) • IABP  IABP decrease myocardial oxygen consumption, increase coronary artery perfusion, decrease afterload and modestly increase cardiac output (0.8–1L/min)  Patients with CS with post AMI mechanical complication  It can be considered in select patients with profound CS when other MCS devices are not available, are contraindicated, or cannot be placed • ECMO  Drainage of venous blood, passing it through an oxygenator and returning the oxygenated blood to systemic circulation using a centrifugal pump  Performed centrally by cannulation of the right atrium and aorta or peripherally with cannulation of the femoral artery and vein  V-A ECMO may be the preferred temporary MCS option when there is poor oxygenation that is not expected to rapidly improve with an alternative temporary MCS device or during CPR
  • 23. • Coronary angiography  The most important investigation in patients diagnosed with CS is coronary angiography  Identify the precise location of the lesion that precipitated CS • PCI strategy  Coronary reperfusion is an essential therapeutic intervention for patients with ACS complicated by CS • Heart transplantation  Cardiac transplantation, particularly for patients requiring biventricular MCS, often represents the only hope for meaningful, long-term recovery. Stabilization and resuscitation strategy
  • 24. • Critically ill patients are at risk of developing complications such as ventilator-associated pneumonia, delirium, ICU-acquired weakness, central line–associated bloodstream infection, stress ulcers, and venous thromboembolism • These complications are associated with an increased risk of morbidity, mortality, and length of stay
  • 25. Reference  Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association. Circulation. 2017;136:e232–e268  Cardiogenic shock: evolving definitions and future directions in management. Open Heart 2019;6:e000960  Cardiogenic Shock. JAHA.2019.119.01199  Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance. Intensive Care Med (2016) 42:147–163  Cardiogenic Shock Classification to Predict Mortality in the Cardiac Intensive Care Unit. JACC. 2019: 2117–28  SCAI clinical expert consensus statement on the classification of cardiogenic shock. Catheter Cardiovasc Interv. 2019;94:29–37  Management of Acute Heart Failure during an Early Phase. Int J Heart Fail. 2020 Apr;2(2):91-110  Epidemiology, pathophysiology and contemporary management of cardiogenic shock. European Journal of Heart Failure (2020) 22, 1315–1341