Birth Emergency Skills Training
Birth Emergency Skills Training
Recognizing Obstetrical Emergencies
By the end of this chapter, you should be able to
Discuss how pregnancy-related changes in cardiovascular function can be mistaken for pathology.
Explain how to use OLDCART to assess pain in a pregnant woman.
List three causes of airway obstruction and discuss how to manage them.
ANTEPARTUM PHYSIOLOGIC ALTERATIONS
Normal changes of pregnancy can mask or mimic pathology, and pathology can mask or mimic normal changes. Profound alterations of maternal anatomy, physiology, and psychology occur during pregnancy, especially with multifetal pregnancies. Most of the physical changes are progressive and relate to either hormonal or physical changes wrought by the developing fetus. Each organ transforms and recovers at its own rate, and some organs never return to their prepregnancy condition. With practice, the body becomes more efficient at maintaining pregnancy; firstborn children average lower birth weights than subsequent children, and even babies born after a first-trimester abortion are generally heavier than babies born to primigravidas.
The healthy woman who conceives with her body mass index in the optimal range will gain roughly 30 lb through the course of her pregnancy. Weight gain includes not only the fetus, but also increased uterine mass, amniotic fluid, placenta, breast glandular tissue, increased extravascular and extracellular fluid, enlarged maternal vital organs, and fat deposition.
Placental hormones affect maternal carbohydrate and lipid metabolism. The goal is to maintain a steady flow of glucose and amino acids to the fetus while supplying extra free fatty acids and glycerol as sources of maternal fuel. Insulin-secreting pancreatic beta cells enlarge and escalate insulin production. Early in pregnancy there is an increased sensitivity to insulin, followed by progressive insulin resistance. Fasting glucose values are 10–20% lower during pregnancy because of decreased hepatic glucose production, increased storage of tissue glycogen, peripheral glucose utilization, and constant glucose consumption by the fetus (Petraglia & D'Antona, 2007). Transient maternal hyperglycemia, often noted following meals, is due to increasing insulin resistance, and transient hypoglycemia before meals and overnight is due to the unrelenting fetal requirements.
Maternal serum cholesterol increases by 50% in pregnancy, and serum triglyceride levels increase by 300%, to provide fuel to mother and fetus (Petraglia & D'Antona, 2007). Lipolysis increases, allowing the mother to burn free fatty acids, triglycerides, and ketone bodies for fuel and reserving more glucose and amino acids for fetal use.
Drug metabolism changes during pregnancy. The increase in body water may dilute medications in the bloodstream, and the decrease in plasma proteins reduces drug binding and may increase serum concentration. Some medications require higher doses to achieve therapeutic serum levels during pregnancy, creating the potential for toxicity after delivery. The gastrointestinal tract moves more slowly during pregnancy, potentially altering drug absorption. Renal filtration rates increase and accelerate excretion of some medications. The second-trimester drop in maternal blood pressure may increase the orthostatic hypotension associated with certain medications such as antipsychotics, tricyclic antidepressants, and antihypertensives.
The fetus and placenta generate large amounts of heat through the process of metabolism. The maternal basal metabolic rate, and therefore heat production, also escalate during pregnancy. The pregnant woman disperses this heat through increased respiration and circulation, increased plasm