Hemorrhagic shock - a condition produced by rapid and significant loss of intravascular volume(hypovolemic), which may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death.

If hypovolemia is severe (40% of the blood volume), the classic signs of shock appear; the blood pressure declines and becomes unstable even in the supine position, and the patient develops marked tachycardia, oliguria, and agitation or confusion.Perfusion of the central nervous system is well maintained until shock becomes severe.
Cerebral blood flow is “autoregulated” extremely well between arterial pressure limits of 60 and 140 mm Hg. That is, mean arterial pressure can be decreased acutely to as low as 60 mm Hg or increased to as high as 140 mm Hg without significant change in cerebral blood flow.
Experiments have shown that a decrease in cerebral tissue PO2 below about 30 mm Hg (normal value is 35 to 40 mm Hg) immediately begins to increase cerebral blood flow. This is fortuitous because brain function becomes deranged at not much lower values of PO2, especially so at PO2 levels below 20 mm Hg. Even coma can result at these low levels.
Anxiety may be related to the release of catecholamines and to mild decreases in cerebral blood flow. A person who is bleeding briskly also may develop tachypnea and hypotension. As hypovolemia worsens and tissue hypoxia ensues, increases in ventilation compensate for the metabolic acidosis produced by increased carbon dioxide production. Compensatory mechanisms are eventually overwhelmed by volume losses, and blood flow to the renal and splanchnic vasculature decreases and systolic blood pressure declines. The loss of coronary perfusion pressure adversely affects myocardial contractility; cerebral blood flow decreases, resulting in the loss of consciousness, coma, and eventually death.
Conditions such as hypercapnia and hepatic and renal failure are associated with a variety of alterations in neurons and astrocytes. The reversible effects of these conditions on the brain are not understood but may result from impaired energy supplies, changes in ion fluxes across neuronal membranes, and neurotransmitter abnormalities.
Reference: Harrison's Internal Medicine > Chapter 268. Coma
Guyton > CHAPTER 61
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