A patient arrives at the hospital emergency department via EMS, complaining of being “lightheaded”. The patient has a heart rate of 42 and BP 90/50 mmHg.

What medication should the RN anticipate being prescribed and administered immediately?

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.

Choice A rationale:

Calcium gluconate is the antidote for magnesium sulfate toxicity. It directly counteracts the effects of magnesium on the neuromuscular system, cardiovascular system, and central nervous system. It is essential to have calcium gluconate readily available at the bedside of any client receiving magnesium sulfate, as toxicity can occur quickly and without warning.

Mechanism of action:

Calcium gluconate competes with magnesium for binding sites on cell membranes and proteins. It displaces magnesium from these sites, thereby restoring normal cellular function.

Calcium gluconate also enhances calcium influx into cells, which further counteracts the effects of magnesium. Indications for use in magnesium sulfate toxicity:

Respiratory depression (respiratory rate <12 breaths per minute) Loss of deep tendon reflexes

Seizures

Cardiac arrhythmias (including heart block and cardiac arrest) Hypotension (systolic blood pressure <90 mmHg)

Dosage and administration:

The typical dose of calcium gluconate for magnesium sulfate toxicity is 1 gram (10 mL of a 10% solution) given IV push over 3- 5 minutes.

This dose may be repeated as needed, depending on the severity of the toxicity and the client's response to treatment. Nursing considerations:

Monitor the client's vital signs, respiratory status, and deep tendon reflexes closely during magnesium sulfate infusion and after administration of calcium gluconate.

Have a crash cart and code equipment readily available in case of cardiac arrest. Document the administration of calcium gluconate and the client's response to treatment.