A nurse is monitoring a laboring client at 40 weeks gestation. The fetal heart rate tracing shows a baseline of 140 bpm with moderate variability. During the last three contractions, the nurse observes late decelerations that begin after the peak of the contraction and return to baseline after the contraction ends. The client's blood pressure is 90/60 mmHg, and she reports feeling dizzy when lying flat. What is the nurse's priority action?

Late decelerations with supine hypotension suggest vena cava compression. Positioning in left lateral relieves this and improves placental blood flow, making it the priority over other interventions.

Understanding the Clinical Picture
The scenario describes a classic case of supine hypotensive syndrome, also known as aortocaval compression. The client is at full term (40 weeks), and the heavy gravid uterus compresses the maternal great vessels when she lies flat. This compression reduces venous return to the heart, leading to decreased cardiac output and maternal hypotension (noted here as 90/60 mmHg) and dizziness. The fetal consequence of this maternal hemodynamic compromise is uteroplacental insufficiency, which manifests on the fetal heart rate (FHR) tracing as late decelerations.

Analyzing the Fetal Heart Rate Pattern
The baseline FHR of 140 bpm with moderate variability is reassuring, indicating that the fetal central nervous system is well-oxygenated and not acidotic at its baseline. However, the presence of late decelerations is a non-reassuring sign. Late decelerations are caused by a transient drop in fetal oxygen saturation during a uterine contraction. In a compromised uteroplacental unit, the contraction further reduces blood flow, and the fetal pO2 drops below a critical threshold, triggering chemoreceptor-mediated vagal slowing of the FHR. The deceleration begins after the peak of the contraction and returns to baseline after the contraction ends, reflecting the time lag in this hypoxic reflex pathway.

Establishing the Priority Action
The nurse’s priority is to correct the underlying cause of the late decelerations. The evidence clearly links the maternal supine position to the observed pathophysiology. A 2025 scoping review by Hammes et al. summarizes that the maternal supine position may reduce uterine and placental perfusion due to compression of the aorta and inferior vena cava, potentially impairing maternal and fetal oxygenation ^[2]. This directly explains the late decelerations seen on the monitor. The client’s report of dizziness and low blood pressure are the maternal clinical correlates of this compression.

Therefore, the immediate and most effective intervention is to relieve the aortocaval compression by repositioning the client. The left lateral position is the standard of care because it shifts the weight of the uterus off the inferior vena cava and aorta, which run along the right side of the vertebral column. This action directly addresses the root cause of the reduced placental perfusion. While administering oxygen (Option 1) and increasing IV fluids (Option 3) are common intrauterine resuscitation measures, they are secondary and supportive. They will be less effective if the primary mechanical obstruction to blood flow is not first removed. Preparing for immediate cesarean delivery (Option 4) is premature; late decelerations caused by maternal position are often completely resolved with a simple position change, and the presence of moderate variability suggests the fetus is not yet in a terminal state of hypoxia. The research by O'Brien and Warland further supports this, noting that maternal supine posture in late pregnancy and labor is known to compromise maternal hemodynamics and subsequently affect the fetus . Repositioning the client to a left lateral position is the definitive first-line nursing action to reverse this sequence of events.