FRCA Notes

Cardiogenic Shock

Resources

  • Cardiogenic shock is a dynamic spectrum of clinical presentations, generally characterised by end-organ hypoperfusion and tissue hypoxia due to primary cardiac dysfunction
  • It may co-exist with other types of shock, e.g. cardiac dysfunction and distributive shock in sepsis
  • It carries a high in-hospital mortality of 40-70%
  • Essentially any cause of heart failure can lead to cardiogenic shock

  • Acute MI with LV dysfunction is the commonest cause; ~9% of patients with acute MI will develop cardiogenic shock
Myocyte death Myocyte dysfunction Circulatory dysfunction Systemic disease
Ischaemic heart disease Cardiomyopathy Acute valve failure Hypo-/hyper-thyroidism
Myocarditis Arrhythmia Aortic dissection Vasculitides
Alcohol β-blocker or CCB overdose Cardiac tamponade Amyloidosis
Cytotoxic drugs Congenital cardiac disease Sarcoidosis
Acidosis Severe, protracted anaemia
Electrolyte disturbance Neuromuscular disease


  • Reduced CO and MAP leads to elevated LV filling pressures
  • High LVEDP reduces coronary perfusion pressure, causing myocardial ischaemia and pulmonary congestion
  • Activation of the RAAS and sympathetic nervous system cause vasoconstriction, sodium and water retention, which may exacerbate the problem

  • A self-perpetuating downward spiral of tissue hypoperfusion, acidosis and congestion ensues
  • This further exacerbates myocardial dysfunction, eventually leading to circulatory collapse and death

  • Some definitions use numerical cardiovascular criteria e.g. certain levels of arterial blood pressure, cardiac index, vasopressor requirement or urine output
  • The Society for Cardiovascular Angiography & Interventions (SCAI) classification is increasingly used as a simple way of describing the stages of cardiogenic shock:
Stage Description Clinical features Mortality
A (at risk) Risk of developing cardiogenic shock but no current clinical features
E.g. recent or new MI		 Normal
SBP typically >100mmHg		 0.8-28.9%
B (beginnings) Haemodynamic instability requiring fluid resuscitation
No organ hypoperfusion		 Warm peripheries, normal capillary refill time and lactate
SBP <90mmHg or MAP <60mmHg
↑ JVP, tachycardia		 2.2-35.1%
C (classic) Organ hypoperfusion requiring intervention beyond fluid resuscitation CI <2.2ml/min/m2
Volume overload e.g. PCWP >15mmHg
Hypoperfusion: ↓ GCS, cool peripheries, ↑ lactate, oliguria, ↑ LFTs		 10.7-59.1%
D (deteriorating) Failure of initial interventions Worsening clinical and biochemical features
Escalating doses of vasoactive interventions
Need for mechanical circulatory support 		24-66.9%
E (extremis ± cardiac arrest) Actual or impending circulatory collapse Unconscious
Profound hypotension/cardiac arrest
Lactate >8mmol/L
pH<7.2
May need CPR or defibrillation		 37.7-85.9%


Ventilatory support

  • Consider non-invasive ventilation e.g. CPAP
  • May need invasive ventilation in order to:
    • Help impaired gas exchange e.g. from pulmonary oedema
    • Facilitate cardiac interventions e.g. PCI
    • Protect the airway of the patient with altered consciousness

Pharmacological cardiovascular support

  • The aim is to restore haemodynamic stability by reversing the pathophysiological spiral

  • No robust evidence for any single inotropic agent over another, althgouh options include:
    • Catecholamines e.g. dobutamine, dopamine, noradrenaline or adrenaline
    • Phosphodiesterase-III inhibitors e.g. milrinone, enoximone
    • Calcium sensitisers e.g. levosimendan

  • Vasoactive management will be guided by invasive haemodynamic monitoring e.g.
    • Intra-arterial blood pressure
    • CVP
    • Cardiac output monitoring e.g. PICCO, LiDCO, PA catheter, TOE
    • Measurements of end-organ perfusion e.g. lactate, urine output

  • Need to ensure:
    • Rate control i.e. HR 80-100bpm, which may include need for pacing
    • Rhythm control, which may include need for cardioversion

Mechanical circulatory support

  • Required in up to 50% of patients, although a proportion of those won't benefit from their use

  • Intra-aortic balloon pump
  • Impella device
  • LVAD
  • VA-ECMO

  • May be used as a bridge to surgery

Interventional cardiovascular support

  • Revascularisation
    • Emergent angiography ± PCI in the patient with known or presumed acute MI causing their cardiogenic shock
    • Immediate revascularisation reduces mortality at 6, 12 and 72 months; delayed revascularisation adversely affects outcomes

  • Surgical
    • Emergency CABG in those unsuitable for or not amenable to PCI
    • For cases where there are mechanical complications of acute MI e.g. severe ischaemic MR
    • Treatment of cardiac tamponade

General supportive care

  • Sedation - consider use of the least haemodynamically worrisome agents
  • Renal - may need RRT as many patients will develop AKI
  • GI - monitoring of liver function as 50% have deranged LFTs, glycaemic control and SUP, consider PN as enteral perfusion may be poor
  • Haem - routine testing of FBC and coagulation, especially as patients may be anticoagulated, transfusion threshold by expert consensus is 9-10g/L (ICM, 2020)