A provider prescribes dextrose 5 The drop factor on the manual IV tubing is 60 gtt/mL. The nurse should set the IV flow rate to deliver how many gtt/min? (Round the answer to the nearest whole number.)

Choice A rationale

Hypocalcemia, defined as a serum calcium level below 9.0 mg/dL (in this case 7.6 mg/dL), typically causes a prolongation of the QT interval on an electrocardiogram, not a shortening. A prolonged QT interval occurs because the phase 2 of the cardiac action potential is extended due to the effect of low calcium on the myocardial cells. Shortened QT intervals are more commonly seen in hypercalcemia, where serum calcium levels exceed 10.5 mg/dL.

Choice B rationale

Constipation is a clinical manifestation of hypercalcemia, which slows gastrointestinal motility and smooth muscle contraction. In contrast, hypocalcemia often leads to increased neuromuscular irritability, which can result in hyperactive bowel sounds or diarrhea rather than constipation. With a calcium level of 7.6 mg/dL, the nurse should expect signs of increased excitability in the nervous system and musculature rather than the depressive effects on the gut seen with high calcium.

Choice C rationale

Hypocalcemia is characterized by neuromuscular irritability and hyperreflexia, meaning the nurse would expect hyperactive deep tendon reflexes. When serum calcium levels drop below 9.0 mg/dL, the threshold for nerve stimulation is lowered, causing muscles to twitch or spasm more easily. Hypoactive reflexes are associated with hypercalcemia or hypermagnesemia, where the excess cations have a sedative effect on the neuromuscular junction, reducing the intensity of the reflex response.

Choice D rationale

Tingling of the extremities, or paresthesia, is a hallmark sign of hypocalcemia. A serum calcium level of 7.6 mg/dL increases peripheral nerve excitability, leading to sensations of numbness and tingling, especially in the fingers, toes, and circumoral area. This occurs because low extracellular calcium levels increase sodium permeability in nerve membranes, causing spontaneous depolarization. This is a critical finding that often precedes more severe symptoms like tetany, Chvostek's sign, or Trousseau's sign.

Choice A rationale

Nystagmus, or involuntary rapid eye movements, is actually a clinical sign associated with hypomagnesemia rather than magnesium toxicity. Low magnesium levels lead to neuromuscular hyperexcitability because magnesium normally acts as a calcium channel blocker; its absence allows for increased acetylcholine release at the neuromuscular junction. Normal serum magnesium levels range from 1.3 to 2.1 mEq/L. Since nystagmus reflects an irritable nervous system, it indicates that the magnesium deficiency has not yet been corrected or has become severe.

Choice B rationale

Kussmaul's respirations are deep, rapid, and labored breathing patterns typically seen in patients with metabolic acidosis, such as diabetic ketoacidosis. This respiratory pattern is a compensatory mechanism to blow off excess carbon dioxide and is not a characteristic finding of hypermagnesemia. In contrast, magnesium toxicity causes central nervous system depression, leading to respiratory depression or a decreased respiratory rate rather than the hyperventilation seen in Kussmaul's. This finding would point toward a different metabolic or acid-base emergency.

Choice C rationale

Lethargy is a hallmark sign of magnesium toxicity, reflecting the sedative effect of high magnesium levels on the central nervous system. As magnesium levels rise above the normal range of 1.3 to 2.1 mEq/L, the mineral acts as a potent depressant. This occurs because excess magnesium inhibits the release of neurotransmitters and reduces the sensitivity of the postsynaptic membrane. If levels continue to rise, this lethargy can progress to a loss of deep tendon reflexes, coma, and cardiac arrest.

Choice D rationale

While magnesium can affect smooth muscle motility, hypoactive bowel sounds are not the primary or definitive indicator of magnesium toxicity used in clinical monitoring. Hypermagnesemia typically causes systemic muscle weakness and vasodilation. A more classic gastrointestinal symptom of magnesium administration is diarrhea, as magnesium acts as an osmotic laxative. The nurse should prioritize assessing neurological status, deep tendon reflexes, and respiratory rate over bowel sounds when specifically monitoring for life-threatening magnesium toxicity during an active intravenous infusion.