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The acidosis that occurs with trauma is secondary to the lack of oxygen for metabolism. When the body begins to use anaerobic metabolism to create ATP, the by-products from that metabolism change from water and CO2 to lactate or lactic acid. [22] The presence of lactic acid in the cells soon begins to lower the intracellular pH and causes the onset of lactic acidosis. [5] pH of 7.28 is indicative of an acidosis.
As the acidotic state persists, the complementary nature of the trauma triad begin to become dangerously apparent. Acidosis inhibits the normal function of the clotting cascade by reducing the action of the enzyme that activates thrombin by 70%.[5] As the patient's pH gets lower, this action becomes increasingly apparent and harder to correct during resuscitation.
The body's compensatory mechanisms to combat metabolic acidosis also make these patients sicker. They attempt to regulate the pH by using the respiratory buffer system in an effort to quickly correct the acidosis. In doing so, they attempt to shift their pH to the alkalotic side by increasing their rate and depth of respiration. This uses an increased amount of oxygen (5-7% more than normal). [22] When acidosis manifests in the presence of hypothermia, its effect is even more detrimental. The body is losing its ability to thermo-regulate, both by losing warm fluids through bleeding and the reduced efficiency of energy production brought on by the anaerobic metabolism. [5] Without adequate energy production, the body cannot generate heat as effectively and the patient quickly becomes hypothermic. This is seen routinely in the current combat theaters of Iraq and Afghanistan, which are arid desert environments where patients are delivered to combat support hospitals in a hypothermic state despite ambient temperatures being well over 105 degrees F.
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