A nurse is caring for a client with dehydration. Which hormonal response should the nurse expect?

Choice A rationale

Autonomic dysreflexia occurs in patients with injuries at or above the T6 level. A noxious stimulus below the injury triggers an exaggerated sympathetic nervous system response. This causes massive vasoconstriction in the lower body, leading to severe hypertension and pale, cool skin. Because the spinal cord injury blocks descending inhibitory signals from the brain, the sympathetic surge remains uncontrolled. The brain attempts to compensate by increasing parasympathetic activity, causing vasodilation and flushing only above the injury level.

Choice B rationale

Decreased norepinephrine release would result in a reduction of sympathetic tone, which typically leads to systemic hypotension rather than the severe hypertension observed in autonomic dysreflexia. In this clinical scenario, there is actually an excessive release of norepinephrine from the sympathetic postganglionic neurons below the level of the spinal cord lesion. This surge is the primary driver behind the sudden and dangerous rise in blood pressure that characterizes this life-threatening neurological emergency.

Choice C rationale

Increased intracranial pressure can lead to Cushing's triad, which includes hypertension, bradycardia, and irregular respirations. While hypertension and bradycardia are present in both conditions, the specific presentation of autonomic dysreflexia is driven by a spinal cord reflex rather than primary brain pathology. The headache and hypertension in this case are secondary to the massive peripheral vasoconstriction and systemic pressure increase, not a primary increase in intracranial volume or pressure within the cranial vault itself.

Choice D rationale

Loss of parasympathetic control would typically result in tachycardia and an inability to achieve vasodilation. However, in autonomic dysreflexia, the parasympathetic nervous system remains intact above the level of the spinal cord injury. The brain sends signals through the vagus nerve to slow the heart and dilate vessels to lower the blood pressure. This explains why the patient experiences flushing and diaphoresis above the injury level while the lower extremities remain constricted and pale.

Choice A rationale

Increased bicarbonate excretion would be an appropriate compensation for metabolic alkalosis, not metabolic acidosis. In metabolic acidosis, the body is experiencing a deficit of base or an excess of hydrogen ions. The renal system attempts to compensate by retaining bicarbonate and excreting hydrogen ions to raise the pH. Excreting more bicarbonate would worsen the acidic state by further depleting the body of its primary buffer system, leading to a dangerous drop in pH.

Choice B rationale

A decreased respiratory rate would lead to the retention of carbon dioxide, which combines with water to form carbonic acid. This process increases the concentration of hydrogen ions in the blood, leading to respiratory acidosis. If a client is already in metabolic acidosis, slowing the breathing would be a maladaptive response that causes a combined acid-base disorder. Respiratory compensation for an acidic state must involve increasing the removal of volatile acids to normalize blood pH.

Choice C rationale

In metabolic acidosis, the body compensates by increasing the respiratory rate and depth, often referred to as Kussmaul respirations. This physiological response facilitates the rapid removal of carbon dioxide from the lungs. Since carbon dioxide acts as a volatile acid in the bloodstream, lowering its partial pressure helps to increase the overall pH back toward the normal range of 7.35 to 7.45. This respiratory compensation occurs quickly to offset the primary metabolic imbalance.

Choice D rationale

Oxygen saturation is a measure of the percentage of hemoglobin binding sites occupied by oxygen and is not a direct compensatory mechanism for acid-base imbalances. While severe acidosis can shift the oxyhemoglobin dissociation curve and affect how easily oxygen is released to tissues, a decrease in saturation does not serve to neutralize excess hydrogen ions. Compensation involves specific adjustments in the partial pressure of carbon dioxide or the concentration of bicarbonate to stabilize pH levels.