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Birth Emergency Skills Training Manual for Out-Of-Hospital Midwives von Gruenberg, Bonnie U. (eBook)

  • Erscheinungsdatum: 24.12.2010
  • Verlag: Birth Muse Press
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Birth Emergency Skills Training

Birth Emergency Skills Training: Manual for Out-of-Hospital Midwives is the interface between the world of midwifery and the world of medicine. It carries the reader from the initial steps of intervention though definitive care, balancing a friendly tone and visual appeal with authoritative and clinically useful information. It is loaded with mnemonics and other memory aids, and is richly illustrated with the author's artful drawings and photography.

Produktinformationen

    Format: ePUB
    Kopierschutz: none
    Seitenzahl: 310
    Erscheinungsdatum: 24.12.2010
    Sprache: Englisch
    ISBN: 9780979002083
    Verlag: Birth Muse Press
    Größe: 8610kBytes
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Birth Emergency Skills Training

Recognizing Obstetrical Emergencies

OBJECTIVES

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.
Metabolism

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.
Thermoregulatory Control

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

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