Shock States in Acute Care Surgery

Abstract

Shock is a condition of insufficient oxygen delivery to the tissues to meet metabolic demands. Shock is not synonymous with hypotension albeit hypotension is almost always associated with shock. Arterial blood pressure, therefore, is not sufficient to diagnose shock. Rather the diagnosis relies on the presence of tissue hypoperfusion (increased arterial blood lactates). With shock, the cellular metabolism is shifted from aerobic to anaerobic. The metabolic consequence of prolonged shock is cellular energy depletion with calcium entry into the cytosol, increased production of reactive oxygen species (ROS), altered membrane permeability and swelling. This causes cellular membrane rupture and death. Subsequent reperfusion of damaged cells contributes to increased ROS production, endothelial barrier disruption with interstitial oedema formation. Ischaemia- reperfusion injury also causes a diffuse inflammatory response with activation of polimorphonuclear neutrophils (PMNs) and production of diffuse organ damage. Haemorrhagic shock is by far the prevalent form of shock in the surgical care setting. Hypovolemia decreases intravascular volume, and anaemia reduces the haemoglobin content so that oxygen supply is severely diminished. The decrease of venous return by reduction of the stressed volume is the main mechanism of hypovolemia in haemorrhagic shock. However, up to 750 mL of blood can be lost without appreciable effects due to the physiological reserve.