A nurse is assessing a client with a recent tissue injury.

Which finding most clearly indicates the client is experiencing a systemic inflammatory response rather than a localized response?

Choice A rationale

Respiratory alkalosis is caused by the excessive loss of carbon dioxide through hyperventilation, resulting in a pH above 7.45. While confusion can occur with any significant acid-base imbalance, the pathophysiology of prolonged vomiting involves the direct loss of hydrochloric acid and potassium from the stomach. This loss of acid leads to an accumulation of bicarbonate in the blood, which is a metabolic process rather than a primary respiratory issue related to CO2 clearance.

Choice B rationale

Metabolic alkalosis is the anticipated imbalance because vomiting results in the significant loss of hydrogen ions and chloride from gastric secretions. As the body loses acid, the serum bicarbonate level increases, raising the pH above 7.45. Confusion arises from electrolyte shifts and reduced cerebral perfusion. Shallow respirations, or hypoventilation, occur as a compensatory respiratory mechanism to retain carbon dioxide, which acts as an acid to help lower the elevated systemic pH.

Choice C rationale

Metabolic acidosis involves a decrease in pH and bicarbonate, often due to the gain of acid or the loss of base, such as in diarrhea or renal failure. Prolonged vomiting has the opposite effect because it removes acid from the body. While severe dehydration from vomiting could eventually lead to poor tissue perfusion and lactic acidosis, the initial and most direct consequence of losing gastric contents is the development of an alkalotic state.

Choice D rationale

Respiratory acidosis is characterized by the retention of carbon dioxide due to hypoventilation, leading to a pH below 7.35. Although the client is currently exhibiting shallow respirations, this is a compensatory response to the primary metabolic alkalosis caused by vomiting. In a primary respiratory acidosis, the client would usually have a history of lung disease or respiratory depression rather than the active loss of acidic gastric fluids seen in this clinical scenario.

Choice A rationale

A stable blood pressure helps maintain the integrity of the blood-brain barrier. The barrier consists of tight junctions between endothelial cells, astrocytes, and a basement membrane. These structures are designed to regulate the movement of substances into the brain parenchyma. When blood pressure remains within a normal autoregulatory range, the physical pressure against these tight junctions is controlled, preventing the mechanical "stretching" or leaking of fluids and solutes into the delicate neural tissue.

Choice B rationale

Normal oxygen saturations, typically maintained above 95 percent, ensure that the endothelial cells of the blood-brain barrier receive adequate oxygen for metabolic processes. Hypoxia, or low oxygen, is what actually threatens the barrier. Under hypoxic conditions, the tight junction proteins can degrade, and inflammatory mediators are released, leading to increased permeability. Therefore, maintaining high oxygen levels is a protective factor that keeps the barrier sealed and functioning as a selective filter for the CNS.

Choice C rationale

A glucose level of 90 mg/dL is within the normal fasting range of 70 to 99 mg/dL. The brain requires a constant supply of glucose, which is transported across the blood-brain barrier via specific GLUT1 transporters. Normal physiological levels of glucose do not disrupt the structural integrity of the barrier. It is chronic hyperglycemia, seen in uncontrolled diabetes, that eventually damages the microvasculature and increases permeability through the formation of advanced glycation end products.

Choice D rationale

Inflammation and infection are primary causes of increased blood-brain barrier permeability. During an infection such as meningitis, pathogens and immune cells trigger the release of proinflammatory cytokines like tumor necrosis factor and interleukins. These substances cause the tight junctions between endothelial cells to loosen. This increased permeability allows white blood cells and antibiotics to enter the brain, but it also permits the entry of toxins and excess fluid, leading to potentially dangerous cerebral edema.