Which of the following would the nurse have readily available for a client who is receiving magnesium sulfate to treat severe preeclampsia?

Rationale for A:

Regular insulin is the only insulin formulation that can be safely administered intravenously. It is a rapid-acting insulin that starts working within 15 minutes and peaks in 1-2 hours, making it ideal for urgent glucose control in situations like diabetic ketoacidosis.

NPH insulin is an intermediate-acting insulin that is not suitable for IV administration. It is designed to be absorbed slowly over several hours, and injecting it intravenously could lead to unpredictable and potentially dangerous fluctuations in blood glucose levels.

Subcutaneous (SQ) injection is the standard route of administration for both regular and NPH insulin outside of acute care settings. This route allows for a more gradual and consistent absorption of insulin, which is essential for maintaining stable blood glucose control.

The patient's transfer to the med/surg unit indicates that their condition has stabilized and no longer requires the aggressive glucose control that is achieved with an IV insulin infusion. Therefore, it is appropriate to transition them to SQ insulin injections.

Rationale for B:

While mixing insulins can potentially alter their absorption rates and action profiles, the primary concern with mixing NPH and regular insulin is not an increased risk of hypoglycemia. It is the incompatibility of the formulations for IV administration.

Rationale for C:

NPH and regular insulin can be mixed together for subcutaneous injection, but they are not compatible for intravenous administration.

Rationale for D:

While NPH insulin can be administered as part of an IV insulin drip in the ICU, this is typically done in specific situations where a continuous infusion of both rapid-acting and intermediate-acting insulin is required. It is not the standard practice for NPH insulin administration.

Choice A rationale:

Dopamine was once considered a first-line vasopressor for cardiogenic shock. However, recent studies have shown that it is associated with increased mortality compared to norepinephrine.

Dopamine has dose-dependent effects on dopamine receptors, beta receptors, and alpha receptors. At low doses (1-5 mcg/kg/min), it primarily stimulates dopamine receptors, leading to renal vasodilation and increased urine output. At moderate doses (5-10 mcg/kg/min), it stimulates beta receptors, resulting in increased heart rate and contractility. At high doses (>10 mcg/kg/min), it stimulates alpha receptors, causing vasoconstriction.

The main concern with dopamine is its potential to cause arrhythmias, particularly at higher doses. This is due to its effects on beta receptors, which can increase heart rate and myocardial oxygen demand.

Additionally, dopamine can cause tachyphylaxis, meaning that its effects can diminish over time, requiring higher doses to achieve the same effect.

Choice B rationale:

Norepinephrine is a potent alpha-adrenergic agonist that causes vasoconstriction, leading to an increase in blood pressure. It has minimal effects on beta receptors, so it is less likely to cause tachycardia and arrhythmias compared to dopamine.

Norepinephrine also has some inotropic effects, meaning that it can increase the strength of contraction of the heart muscle.

Studies have shown that norepinephrine is associated with improved survival rates in patients with cardiogenic shock compared to dopamine.

It is generally well-tolerated, with the most common side effects being hypertension and peripheral vasoconstriction.

Choice C rationale:

Epinephrine is a potent alpha- and beta-adrenergic agonist that causes vasoconstriction, increased heart rate, and increased contractility.

It is typically used as a second-line agent in cardiogenic shock, after norepinephrine has failed to achieve adequate blood pressure.

Epinephrine can cause significant tachycardia and arrhythmias, so it should be used with caution in patients with underlying heart disease.

Choice D rationale:

Vasopressin is a hormone that causes vasoconstriction by acting on V1 receptors in vascular smooth muscle. It is sometimes used as an adjunct to norepinephrine in patients with refractory cardiogenic shock.

Vasopressin has the potential to cause coronary vasoconstriction, so it should be used with caution in patients with coronary artery disease.