Milo, a 19-year-old, lives in an inner-city apartment complex. One late night he was walking home after hanging out with his friends
Before he knew what was happening, someone jumped Milo from behind and tried to get his wallet. A fight broke out, and the thief stabbed Milo in the abdomen before taking off. When the paramedics arrived, Milo was pale, sweating, and rolling restlessly on the ground. His pulse was 94 beats/minute and his blood pressure 115/82 mm Hg. He was rushed to the hospital where his treatment began immediately.
Why is Milo presenting with pallor, diaphoresis, and restlessness?
In spite of his blood loss, Milo's blood pressure was only slightly affected when the paramedics first found him. Describe how cardiovascular compensatory mechanisms serve to maintain homeostasis as long as possible in the early stages of shock. How does ADH contribute to compensation?
What are the disadvantages of prolonged vasoconstriction in hypovolemic shock?
If Milo's respirations were to become progressively deeper and more rapid, what physiological changes in the body would that indicate?
Hypovolemia creates a sympathetic response in the body in an attempt to maintain homeostasis in the presence of fluid loss. Increased sympathetic activity stimulates sweat gland activity and generates restlessness. The sympathetic response also causes vasoconstriction of the dermal vasculature. In concert with a decline in red blood cells, the skin and mucous membranes appear pale as a result.
The heart, under sympathetic influence, beats faster and with greater contractility as a means to maintain homeostasis in the presence of fluid loss. Arteriolar constriction occurs to ensure systemic resistance, while venous constriction ensures venous return to the heart. An added benefit of venous constriction is the movement of blood that has been stored in the capacitance portion of the circulation. Fluid loss also stimulates the release of ADH from the posterior pituitary. ADH stimulates thirst centers in the hypothalamus and assists in the generation of peripheral vasoconstriction. It also has a strong effect on the kidneys and stimulates water resorption by renal tubules.
As fluid loss continues, vasoconstriction intensifies as a means to maintain vascular resistance and perfusion to the major organs. Prolonged vasoconstriction, however, limits tissue perfusion and oxygenation. Tissue cells revert to anaerobic metabolism, which over time leads to lactic acid production and cellular damage.
Increased rate and depth of respirations indicate the presence of metabolic acidosis, a result of the shift from aerobic to anaerobic cellular respiration. A decrease in the oxygen-carrying capacity of the blood (due to volume loss) is an additional factor for the alteration in ventilation.
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