Shock

Overview
  • Shock results when the circulatory system cannot deliver sufficient perfusion to meet the metabolic demands of the body
Pathogenesis
  • Systemic Arterial Pressure is ultimately dependent on sufficient Cardiac Output (CO) and sufficient Systemic Vascular Resistance (SVR) (Discussed in Systemic Arterial Pressure Regulation. Shock-inducing processes result in the failure of one of these factors: CO or SVR. Whichever hemodynamic variable fails (CO or SVR), a variety of compensatory mechanisms are activated which attempt to maintain systemic arterial pressure by boosting the other, intact variable. If such compensatory mechanisms are insufficient, systemic hypotension ensues which leads to widespread hypoperfusion and thus reduced delivery of metabolic resources to multiple organs.
  • As hypoperfused organs undergo hypoxia, they switch their metabolism to anaerobic glycolysis and release metabolites such as lactic acid. These metabolites not only produce a metabolic acidosis characteristic of shock but also activate mechanisms designed for local blood flow regulation on an inappropriate, system-wide scale which causes systemic arteriolar vasodilation and thus further drops SVR. If hemodynamic derangements continue, infarction and consequent dysfunction of sensitive organs ensues, resulting in an irreversible spiral towards death.
Clinical Consequences
  • Overview
    • The clinical consequences of shock depend in part on the etiology. When the disease process causes dysfunction of CO, the pulse pressure will be weak while severe compensatory peripheral vasoconstriction will manifest as cold, pale, and sweaty extremities. When the disease process causes inappropriate drops in SVR, then extremities will be warm and red whereas compensatory increases in CO will manifest as tachycardia. Whatever the proximate cause of shock, hypoperfusion results in characteristic pathology in several important organs as listed below.
  • Organ-specific Consequences
Etiological Subtypes
  • Overview
    • Shock has been divided into several prototypical etiological subtypes. In each case, the cause of shock will primarily be either a severe insult to CO or SVR. Additionally, compensatory physiological mechanisms will be different in each case corresponding to which organ systems are still intact after the proximate insult.
  • Subtypes