A client has a systolic blood pressure of over 200 mm Hg and a severe headache.
The physician orders a nicardipine infusion. What should the nurse explain to the family about the use of this medication?
It will increase heart rate to improve cardiac output.
It will relieve the pain of the headache by stimulating endorphins.
It will rapidly lower blood pressure to prevent stroke or bleeding.
It will promote fluid loss to decrease blood pressure.
The Correct Answer is C
Management of hypertensive crisis involves using calcium channel blockers to achieve rapid vascular relaxation. Knowledge of pharmacodynamics is necessary to explain how nicardipine reduces systemic vascular resistance to mitigate the risk of cerebrovascular accidents and end organ damage in emergencies.
Choice A rationale
Nicardipine is a dihydropyridine calcium channel blocker that primarily causes vasodilation. It does not act as a positive chronotrope. Increasing heart rate in a hypertensive crisis could dangerously increase myocardial oxygen demand and exacerbate the clinical situation.
Choice B rationale
The medication does not possess analgesic properties or stimulate endorphin release. While the headache may improve as intracranial pressure decreases from lowered blood pressure, the primary pharmacological mechanism is vascular smooth muscle relaxation rather than pain modulation.
Choice C rationale
Nicardipine inhibits calcium ion influx into vascular smooth muscle, leading to rapid peripheral vasodilation. In a hypertensive emergency (BP > 180/120 mm Hg), quick reduction is critical to prevent intracranial hemorrhage, encephalopathy, or ischemic stroke.
Choice D rationale
Nicardipine does not function as a diuretic. While lowering blood pressure reduces renal strain, it does not promote fluid loss through the kidneys. Diuretics like furosemide are separate agents used for volume related hypertension or edema.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is ["A","C","D"]
Explanation
This case involves phenytoin toxicity resulting from a level exceeding the therapeutic range of 10 to 20 mg/dL. Knowledge of central nervous system effects, pharmacokinetics, and toxicological manifestations of anticonvulsants is necessary to identify appropriate neurological assessment findings.
Choice A rationale
Nystagmus, or involuntary eye movement, is a classic sign of phenytoin toxicity as levels rise above 20 mg/dL. It results from the drug's effect on the cerebellum and vestibular system, disrupting normal extraocular muscle coordination and balance.
Choice B rationale
Phenytoin typically causes hyperglycemia rather than hypoglycemia because it inhibits insulin secretion. A serum level of 32 mg/dL would not be expected to lower blood glucose; monitoring for elevated glucose levels is more appropriate in toxicity.
Choice C rationale
Ataxia involves uncoordinated muscle movements and gait instability, frequently occurring when phenytoin levels exceed therapeutic limits. The drug affects cerebellar function, leading to significant motor impairment and increasing the client's risk for falls and physical injury.
Choice D rationale
Vertigo or dizziness is a common central nervous system side effect of high phenytoin concentrations. As the drug reaches toxic levels like 32 mg/dL, it interferes with vestibular signaling, causing the sensation of spinning or loss of balance.
Choice E rationale
Phenytoin toxicity is more likely to cause blood dyscrasias like leukopenia or thrombocytopenia rather than a high platelet level. Normal platelet counts are 150,000 to 400,000 cells/mm; high levels are not a recognized manifestation of phenytoin overdose.
Correct Answer is A
Explanation
Pulmonary embolism disrupts the ventilation-perfusion ratio, leading to sudden hypoxemia and respiratory distress. Prioritizing interventions requires applying the airway, breathing, circulation framework. Knowledge of gas exchange and emergency protocols is necessary to stabilize the client and maintain systemic cellular oxygenation.
Choice A rationale
Oxygen administration is the priority to treat hypoxemia caused by the physiological dead space created by the embolism. Improving arterial oxygen saturation supports myocardial and cerebral function while reducing the workload of the right ventricle during obstruction.
Choice B rationale
Morphine acts as an analgesic and vasodilator which can reduce anxiety and preload. However, it does not address the primary physiological threat of impaired gas exchange. Breathing and oxygenation must be stabilized before managing pain or sedation.
Choice C rationale
Cardiac monitoring identifies arrhythmias and right-sided heart strain associated with pulmonary hypertension. While diagnostic, it is a secondary action that follows the restoration of oxygenation. Assessment tools should not delay the implementation of life-saving oxygen therapy.
Choice D rationale
Lactated Ringer's is used for volume expansion and electrolyte replacement. In pulmonary embolism, excessive fluid can worsen right ventricular failure and pulmonary edema. Circulatory support is important but remains secondary to correcting the immediate life-threatening respiratory deficit..
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