A client asks about nutritional needs in pregnancy. Which should the nurse include? Select all that apply

Supine hypotensive syndrome occurs when the gravid uterus exerts pressure on the inferior vena cava and descending aorta. This mechanical compression reduces venous return to the maternal heart, subsequently decreasing cardiac output and systemic perfusion. Obstruction of these major vessels compromises the hemodynamic stability of both mother and fetus.

A. The supine position increases BP: In reality, this position typically causes a precipitous drop in maternal blood pressure due to reduced stroke volume. While some patients may experience a brief compensatory heart rate increase, the primary vascular effect is systemic hypotension. It does not cause a hypertensive state in the pregnant patient.

B. The supine position causes contractions: Uterine activity is generally independent of maternal posture, although severe hypotension could theoretically cause fetal distress that triggers labor. However, there is no direct physiological link between lying flat and the initiation of uterine contractions. Positioning is managed for vascular reasons rather than labor prevention.

C. The supine position reduces uterine blood flow: Compression of the aorta and iliac arteries directly impairs placental perfusion, potentially leading to fetal bradycardia or late decelerations. Maternal hypotension further reduces the pressure gradient necessary for efficient gas exchange at the intervillous space. Avoiding this position is critical for maintaining fetal oxygenation.

D. The supine position causes nausea: While some women may feel nauseated due to sudden hypotension and reduced cerebral blood flow, this is a subjective symptom rather than the primary medical concern. The core risk is the vascular compromise to the fetus. Clinical teaching focuses on the circulatory risks rather than gastrointestinal discomfort.

Hyperemesis gravidarum is a severe complication characterized by intractable vomiting leading to fluid-electrolyte imbalance, ketonuria, and weight loss exceeding 5% of pre-pregnancy mass. The pathophysiology involves high serum hCG levels and potential hyperthyroidism. Patients exhibit signs of intravascular dehydration and metabolic alkalosis.

A. Iron deficiency: While anemia is common in pregnancy, it typically presents with fatigue and pallor rather than acute, persistent emesis and significant weight loss. Iron supplements can actually exacerbate gastric irritation and nausea. It is not the primary cause of the severe hemodynamic instability described here.

B. Hyperemesis gravidarum: The combination of 6-pound weight loss, persistent inability to retain nutrients, and orthostatic dizziness indicates a pathological state beyond normal morning sickness. This condition requires aggressive intravenous rehydration and electrolyte replacement. Dark urine and dizziness are clinical hallmarks of severe volume depletion.

C. Gastroenteritis: An acute infection of the digestive tract usually presents with diarrhea, fever, and abdominal cramping alongside vomiting. While it causes temporary dehydration, the 10-week gestational timing and lack of lower gastrointestinal symptoms point toward a pregnancy-induced etiology. It is typically a self-limiting viral or bacterial event.

D. Normal morning sickness: Physiological nausea of pregnancy usually peaks in the morning and does not result in significant weight loss or clinical dehydration. Clients can typically maintain some oral intake and do not experience dizziness upon standing. It lacks the severe metabolic consequences seen in hyperemesis.