A patient receiving hydralazine IV for severe preeclampsia develops tachycardia and headache. What is the appropriate nursing action?

Hydralazine adverse effects are common during intravenous administration, especially in obstetric patients with severe preeclampsia. Hydralazine is a direct arteriolar vasodilator used to lower diastolic blood pressure rapidly. It acts by relaxing vascular smooth muscle, leading to decreased systemic vascular resistance. However, this vasodilation can trigger reflex sympathetic activation, resulting in tachycardia, headache, and palpitations. These symptoms may indicate excessive hypotension or cerebral vasodilation, both of which are dangerous in preeclampsia. Hydralazine is contraindicated in patients with tachyarrhythmias, angina, or increased intracranial pressure.

Rationale for correct answer

1. Stopping the medication and notifying the provider is appropriate because tachycardia and headache suggest adverse effects from hydralazine-induced vasodilation. These symptoms may reflect excessive hypotension or cerebral hyperperfusion, both of which can worsen maternal and fetal outcomes. Immediate cessation prevents further hemodynamic instability.

Rationale for incorrect answers

2. Continuing the infusion and reassessing in 30 minutes is unsafe. Tachycardia and headache are not mild side effects but signs of hemodynamic stress. Delaying intervention risks progression to hypotension, fetal compromise, or stroke. Reassessment without action is inappropriate.

3. Administering another antihypertensive without evaluating the cause of symptoms may worsen the situation. Combining agents can lead to synergistic hypotension and further cardiac strain. The priority is to stop the offending drug and reassess before initiating new therapy.

4. Documenting and continuing observation ignores the clinical significance of the symptoms. Headache in preeclampsia may signal cerebral edema or vasospasm, and tachycardia may indicate compensatory response to hypotension. Passive observation delays necessary intervention.

Take home points

• Hydralazine causes reflex tachycardia and headache due to arteriolar vasodilation.
• These symptoms may indicate excessive hypotension or cerebral hyperperfusion.
• Immediate cessation and provider notification are required for adverse reactions.
• Monitoring for neurological and cardiovascular signs is critical in preeclampsia.

Magnesium sulfate toxicity occurs when serum magnesium levels exceed the therapeutic range of 4.8–8.4 mg/dL, leading to progressive neuromuscular and respiratory depression. Magnesium acts as a calcium antagonist at neuromuscular junctions, reducing acetylcholine release and impairing muscle contraction. Early signs include loss of deep tendon reflexes, followed by respiratory depression (rate <12 breaths/min), and eventually cardiac arrest. Magnesium is excreted renally, so decreased urine output increases the risk of accumulation. Monitoring reflexes, respiratory rate, and urine output is essential to detect toxicity early.

Rationale for correct answers

1. Loss of deep tendon reflexes is an early and reliable indicator of neuromuscular blockade due to magnesium’s inhibitory effect on acetylcholine release. It precedes respiratory depression and signals rising serum magnesium levels.

2. Respiratory rate <12 breaths/min reflects respiratory muscle paralysis from excessive magnesium. Magnesium depresses the medullary respiratory center, leading to hypoventilation and potential apnea.

3. Decreased urine output (<30 mL/hour) impairs renal clearance of magnesium, increasing the risk of toxic accumulation. This is especially dangerous in preeclamptic patients with renal involvement.

Rationale for incorrect answers

4. Hyperreflexia is not a sign of magnesium toxicity. It is typically seen in preeclampsia before magnesium administration. Magnesium suppresses reflexes; thus, hyperreflexia suggests subtherapeutic levels, not toxicity.

5. Increased blood pressure is a hallmark of preeclampsia, not magnesium toxicity. Magnesium sulfate does not raise blood pressure; it may cause vasodilation and mild hypotension. Elevated pressure indicates disease severity, not drug toxicity.

Take home points

• Magnesium toxicity presents with hyporeflexia, respiratory depression, and reduced urine output.
• Reflex monitoring is essential for early detection of toxicity.
• Hyperreflexia suggests subtherapeutic magnesium levels.
• Magnesium is excreted renally; oliguria increases toxicity risk.