Shock

An abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation - can lead to anaerobic metabolism, which will cause metabolic waste products to accumulate, resulting in cellular failure

Hypovolemic Shock

  • Shock due to decrease in blood volume
  • Decrease can be either due to:
    • Haemorrhage - direct blood loss (e.g. trauma, surgery, GI haemorrhage)
      • Classified into 4 classes (IV most severe) depending on different factors e.g. blood loss, pulse pressure, BP, resp. rate etc.
    • Non-haemorrhage - decrease in ECFV e.g. due to vomiting, diarrhoea, excessive sweating

Pathophysiology

  • Decrease in blood volume → decreased venous return → decreased EDV → decreased SV (Frank-Starling) → decreased CO and BP → inadequate tissue perfusion

Compensatory cardiac mechanisms

  • Can maintain BP until >30% of blood volume is lost
  • In haemorrhagic shock, the baroreceptor reflex will cause the patient to become tachycardic, decreasing SV → CO and MAP decreases
  • SVR will increase through vasocontraction - cool peripheries
    • Myogenic response - the intrinsic ability of smooth muscle to alter SVR in response to pressure changes e.g. to regulate cerebral blood flow in response to decreased MAP

Cardiogenic Shock

  • Decreased cardiac contractility (e.g. due to acute MI) → decreased stroke volume → decreased CO and BP → inadequate tissue perfusion

Obstructive Shock

  • Shock associated with physical obstruction of the great vessels or the heart itself
  • Includes cardiac tamponade, pulmonary embolism and tension pneumothorax

In the case of a tension pneumothorax:

  • Increased intrathoracic pressure → decreased venous return → decreased EDV → decreased SV (Frank-Starling) → decreased CO and BP → inadequate tissue perfusion

Distributive Shock

Neurogenic e.g. spinal cord injury

  • Loss of sympathetic tone to blood vessels and heart → massive venous and arterial dilation and heart rate slows → decreased venous return and SVR → decreased CO and BP → inadequate tissue perfusion

Vasoactive shock e.g. septic shock, anaphylactic shock

  • Release of massive vasoactive mediators → massive venous and arterial vasodilation, increased capillary permeability → decreased venous return and SVR → decreased CO and BP → inadequate tissue perfusion

Management

  • ABCDE approach
  • High flow oxygen
  • Volume replacement for hypovolaemic shock
  • Inotropes for cardiogenic shock
  • Immediate chest drain for tension pneumothorax
  • Adrenaline for anaphylactic shock
  • Vasopressors for septic shock
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