The provider orders an infusion of oxytocin to prevent postpartum hemorrhage at 20 mU/min.

The availability of the oxytocin infusion is 20 units/1000 mL of normal saline.

How many mL/hr will the oxytocin infuse. (Record numerical answers only. Round the answer to the nearest whole number.)

Choice A rationale

Insulin resistance is a physiological change occurring in the second and third trimesters, primarily induced by placental hormones like human placental lactogen (hPL), progesterone, and cortisol. These hormones antagonize insulin action at the cellular level, necessitating higher insulin doses to maintain euglycemia. The normal fasting blood glucose is <95 mg/dL and 1-hour postprandial is ≤ 140 mg/dL.

Choice B rationale

The fetus produces its own insulin by approximately 10 weeks gestation and is not dependent on maternal insulin to regulate its blood glucose. Maternal insulin does not cross the placenta due to its large size. Glucose, however, does cross, and maternal hyperglycemia causes fetal hyperinsulinemia and subsequent fetal macrosomia.

Choice C rationale

While circulating blood volume significantly increases (by 30-50%) during pregnancy, leading to some hemodilution, this is not the primary mechanism for increased insulin requirements. The main mechanism is the anti-insulin effect of the aforementioned placental hormones that induce peripheral insulin resistance.

Choice D rationale

While dietary intake and carbohydrate metabolism shift during pregnancy, the major underlying cause for the escalating insulin need is the hormonally mediated increased insulin resistance. Nutritional adjustments are made, but they do not independently cause the progressive need for doubling or tripling of the usual pre-pregnancy insulin dose.

Choice A rationale

Uterine atony is the leading cause of postpartum hemorrhage, resulting in significant blood loss and hypovolemia. Increasing intravenous fluid replacement with crystalloid solutions (e.g., normal saline or lactated Ringer's) is critical to restoring circulating blood volume, maintaining hemodynamic stability, and preventing hypovolemic shock.

Choice B rationale

A full bladder can displace the uterus and impede its ability to contract effectively, contributing to or worsening uterine atony. Inserting an indwelling urinary catheter (Foley catheter) ensures continuous bladder drainage and decompression, allowing the uterus to move into its proper place and contract more effectively.

Choice C rationale

Monitoring deep tendon reflexes (DTRs) is primarily an assessment for magnesium sulfate toxicity in clients being treated for preeclampsia or eclampsia. While relevant in those specific conditions, it is not a direct intervention for managing the immediate effects or cause of postpartum hemorrhage due to uterine atony. Normal DTR response is 2+.

Choice D rationale

Quantifying blood loss is essential for determining the severity of the hemorrhage and the efficacy of interventions. Initiating a peri-pad count and accurately weighing the pads provides a reliable, though often underestimated, measure of blood loss, guiding the need for additional fluids, blood products, or uterotonic medications.

Choice E rationale

Uterine atony is a failure of the uterine muscle to contract and compress the blood vessels at the placental site. Performing a fundal massage stimulates the myometrium to contract, thereby physically compressing the vessels and activating the natural physiological mechanisms to stop the bleeding; this is a primary, initial intervention.

Choice F rationale

Tocolytic therapy, such as terbutaline or nifedipine, works by relaxing the uterine muscle, which is used to stop preterm labor. In the context of uterine atony, the goal is to contract the uterus, so administering tocolytic therapy would be contraindicated as it would worsen the atony and accelerate blood loss.