Refractory shock

[Ref: BL8:p283-285; WG21:p642]

 

Characterised by positive feedback

Acidosis

Decreased perfusion may lead to increase anaerobic glycolysis, resulting in lactic acidosis

Resulting in:

• Depression of myocardium
• Reduced reactivity of heart and resistance vessels to catecholamine

--> Aggravate fall in BP

Heart failure

• Reduced coronary blood flow
  * Despite maximal dilation of coronary vessels
  * Due to hypotension and tachycardia
• Accumulation of vasodilator metabolites in periphery
  --> Further aggravate fall in BP

 

Severe CNS ischaemia

Depression of cardiovascular centres in the brainstem

--> Reduced sympathetic tone

--> Drop in BP

 

Alterations in coagulation

• Initial phase of hypercoagulability is followed by...
• Late phase of hypocoagulability and fibrinolysis

--> Further bleeding and drop in BP

 

Depression of reticuloendothelial system

Endotoxins from normal bacteria flora in intestines are normally inactivated by RES, mainly in the liver

When RES is depressed, endotoxins invade the circulation

--> Produce profound generalised vasodilation

 

Other notes

Acute respiratory distress syndrome

Late complication of shock

Damage to capillary endothelial cells and alveolar epithelial cells

--> Release of cytokines