Cardiogenic shock is a life-threatening condition occurring in 4-15% of acute myocardial infarction cases, with a high mortality rate of 50%. It is defined as impaired organ perfusion due to reduced cardiac output and low blood pressure. Treatment involves general supportive measures, inotropic drugs, revascularization procedures, and mechanical circulatory support devices to increase blood pressure and cardiac output. With early reperfusion therapy and intensive care, mortality from cardiogenic shock complicating acute coronary syndrome can be reduced to around 40%.

1. CARDIOGENIC SHOCK
Department of Cardiology
Yangon General Hospital

2. SCOPE
1. Introduction
2. Definition
3. Causes
4. Pathophysiology
5. Risk factors and Prognosticators
6. Treatment

3. INTRODUCTION
 Incidence of cardiogenic shock (CS) in patients
with acute myocardial infarction (AMI) - 4% to 15%
 Hospital mortality rates - 50%
 Related to old age, higher risk profile, the disease
burden and multiple co-morbidities

4. DEFINITION
 A state of impaired end-organ perfusion, due to a
reduced cardiac output characterized by
hypotension, pulmonary congestion, impaired
tissue and vital organ perfusion
 Additional haemodynamic parameters; left
ventricular (LV) filling pressures or cardiac index
can be used

5. CRITERIA OF CS
 Systolic blood pressure <90 mmHg for >30 min or
vasopressors required to achieve ≥90 mmHg
 Pulmonary congestion or elevated LV filling pressures
 Signs of impaired organ perfusion with at least one of the
following criteria:
 Altered mental status
Cold, clammy
 Oliguria
 Increased serum lactate
 Reduced cardiac index (<1.8 L/min/m2 without support,
and 2.0–2.2 L/min/m2 with support) (optional)

6. ETIOLOGIES ( 1 )
 Acute Myocardial Infarction
 LV Failure, VSR, Papillary muscle rupture, Free wall
rupture
 Post Cardiac Arrest
 Post Cardiotomy
 Refractory Sustained Tachy- and Brady-arrhythmia
 Acute Fulminant Myocarditis
 End-stage Cardiomyopathy
 HOCM with severe outflow obstruction
 Aortic dissection with tamponade
 Massive pulmonary embolism

7. ETIOLOGIES ( 2 )
 Severe Valvular Heart Disease
 Critical aortic or mitral stenosis
 Acute severe AR or MR
 Toxic metabolic
 Beta blocker or CCB overdose
 Severe acidosis, severe hypoxaemia
 RV Failure due to AMI or Acute corpulmonale
 Pericardial tamponade

8. PATHOPHYSIOLOGY
 Profound depression of myocardial contractility,
resulting in a vicious spiral of reduced cardiac
output, low BP, further coronary ischaemia, &
subsequent reduction in contractility & cardiac
output, leading to death, if not interrupted by
adequate treatment.
 Loss of LV function is the major cause, with
subsequent systolic and diastolic dysfunction

9.  Extremity and vital organ hypoperfusion is the hallmark
 Compensation mechanisms by vasoconstriction lead to an
intermittent improvement in the coronary and peripheral
perfusion, with increased afterload.
 Vasoconstriction followed by systemic inflammation,
leading to subsequent pathologic vasodilatation with
increasing shock duration.
 Increased endothelial and inducible NO synthase with high
NO levels, peroxynitrite , Ils, TNF - cardiac toxic and
negatively inotropic

10. PATHOPHYSIOLOGY

11. DIAGNOSIS
 Supportive therapy must be initiated
simultaneously with diagnostic evaluation since
unstable condition of patients
 Focused history and physical examination, basic
blood test (including cardiac enzymes), ECG, CXR
 2D echo with doppler is invaluable ( for tertiary
center )

12. CLINICAL FINDINGS
 Continuing chest pain
 Dyspnea
 Pale &cyanotic
 Diaphoretic
 Altered mentation
 Varying degrees of somnolence & confusion
 Hypoxemia and metabolic acidosis

13. RISK FACTORS & PROGNOSTICATORS
CARDSHOCK Score
1. Age >75 years (1 point),
2. Confusion at presentation (1 point),
3. Previous infarction or CABG (1 point),
4. Aetiology of ACS (1 point),
5. Ejection fraction <40% (1 point),
6. Serum lactate (<2 mmol/L [0 point], 2–4 mmol/L [1
point], >4 mmol/L [2 points]), and
7. eGFR (>60 mL/min [0 point], 30–60 mL/min [1 point],
<30 mL/min [2 points]) results in a maximum score of 9.
 The predicted mortality ranges from 15% for a score of 2
and close to 100% for a score of 9

14. IABP-SHOCK II score

15. TREATMENT
 General Measures
 Initial therapy – to raise systolic blood pressure to
90 mmHg with vasopressors and adjusting volume
status (optimum LV filling pressure - PCWP 20
mmHg)
 Correct hypoxemia and acidosis, may need
endotracheal intubation
 Discontinue negative inotropic agents

16.  Correct hyperglycemia - with continuous insulin
infusion
 Transvenous pacing for bradycardia
 Immediate cardioversion for recurrent ventricular
tachycardia or rapid atrial fibrillation

17.  3 primary clinical objectives in the setting of AMI complicated by CS.
 Circulatory support is defined by an increase in mean arterial pressure.
 Ventricular support is defined by a reduction in LV pressure and volume, thereby
reducing myocardial wall stress and oxygen demand.
 Coronary perfusion is defined by an increase in the trans-myocardial gradient, which
is determined by the difference between coronary arterial and LV end-diastolic
pressure.
 The net effect of optimal hemodynamic support is increased urine output, reduced
serum lactate, reduced pulmonary capillary wedge pressure, resolution of ischemic
ECG changes, and reduced levels of myocardial injury biomarkers such as creatine
kinase-MB.

18. Treatment of CS
1. Adjunctive medical treatment - Inotropes
2. Revascularization – PCI or CABG
3. Percutaneous mechanical support
4. Treatment of mechanical complications of AMI

19. Catecholamines
 Norepinephrine is preferred over dopamine
 Norepinephrine - titrated, until the SBP rises to at least 80
mmHg
 Subsequently, IV dobutamine, due to its β2-adrenergic effects,
given simultaneously, to improve cardiac contractility
 Not produce consistent improvement in symptoms and
shortened the survival
 May be related to - increase myocardial oxygen consumption,
concentrations of cyclic adenosine monophosphate (cAMP),
producing an increase in intracellular calcium leading to
myocardial cell death and/or increases lethal arrhythmias.

21. PERCUTANEOUS MECHANICAL SUPPORT

23. SUMMARY
 CS complicating ACS in 10% of patients with high
mortality 50%.
 Extent of ischaemic myocardium - profound impact on the
initial, in-hospital, and post-discharge management and
prognosis
 Careful risk assessment is mandatory
 Crucial importance for a multidisciplinary team
management and a specialized centre to improve clinical
outcome
 With an early reperfusion for all patients and an optimal
intensive care treatment, mortality can reduced to 40%.

24. The End