Fetal anoxia

If contractions are frequent, prolonged, or excessive, die infusion is stopped to prevent fetal anoxia or trauma to die uterus. Excessive stimulation of die uterus can cause uterine hypertonicity and possible uterine rupture. The nurse places die patient on her side and provides supplemental oxygen. The effects of die drug diminish rapidly because oxytocin is short acting. 

Uses Mydriasis, ocular redness [OTC], pmop mydriasis, postmor synechiae, uveitis w/ postmor S5mechiae Action a-Adren gic agonist Dose Adults. Redness 1 gtt 0.12% q3-4h PRN Exam mydriasis 1 gtt 2.5% (15 min-1 h for effect) Preop 1 gtt 2.5-10% 30-60 min preop Ocular disorders 1 gtt 2.5-10% daily-tid Peds. As adult, only use 2.5% for exam, preop, and ocular conditions Caution [C (may cause late-tOTn fetal anoxia/bradycardia), +/-] HTN, w/ elderly w/ CAD Contra NAG Disp Ophth soln SE Tearing, HA, irritation, eye pain, photophobia, arrhythmia, tremor EMS None OD Unlikely but may cause exaggeration of nl SEs s5rmptomatic and supportive... 

Everrts leading to abortion often take place we or nronths prior to the expulsion of the fetus, and the agent may not be present or detectable in the conceptus at the time of abortion. For example, abortion from nitrites results from fetal anoxia secondary to methemoglobinemia. By the time the fetus is expelled from die uterus, the hemoglobin has returned to normal. 

The fetoplacental unit includes maternal and fetal placental circulations, other placental functions, umbilical cord and amniotic fluid. If chemicals — for example, vasoactive drugs — reduce the placental circulation or cause umbilical vasoconstriction, then marked prolonged action may cause fetal death from anoxia, but an action for less than 2 h in rodents may cause fetal growth retardation or... 

FIGURE 10—34. Neurodegenerative causes of schizophrenia may lead to a final common pathway either of neuronal death or possibly of destruction of synapses and the axons and dendrites of such synapses. The causes can range from predetermined genetic programming of neuronal or synaptic destruction to fetal insults such as anoxia, infection, toxins, or maternal starvation to perhaps a destructive effect of the positive symptoms themselves on synapses and neurons via glutamate-mediated excitotoxicity. 

GHB is gaining popularity in France and Italy as an aid in childbirth because it induces remarkable hypotonia, or muscle relaxation.40 GHB has been reported to cause spectacular action on the dilation of the cervix, decreased anxiety, greater intensity and frequency of uterine contractions, and increased sensitivity to drugs used to induce contractions. It also produces a lack of respiratory depression in the fetus, and protection against fetal cardiac anoxia (lack of oxygen to the heart, especially in cases where the umbilical cord wraps around the fetus s neck).41... 

Unhke that of the adult, fetal metabolism is geared toward tissue accretion and maturation in preparation for birth (109) however, like the adult, there is an absolute requirement for oxidative metabolism to achieve these ends. The fetus, especially in early to midgestation, has a much lower metabohc rate than its adult counterpart (Fig. 4) and yet, unlike the adult, the fetus is capable of withstanding prolonged periods of profound hypoxia and anoxia. 

A more detailed study of [Ca " "] response maturation was undertaken in clusters of type 1 cells isolated from near-term fetal rats and rats 1,3,7, 11, 14, and 21 days old (68). The [Ca " "] response to maximal hypoxic stimulation (anoxia) was low in term-fetal cells and increased with age (Fig. 3), consistent with previous CSN recordings both in vivo (11,14) and in vitro (10,12,45). In addition, the submaximal portion of the type I cell O2 response curve for [Ca ]i increased approximately fourfold during postnatal development (Fig. 4). Thus, as with afferent nerve activity, graded maximal and submaximal type I cell [Ca ]i responses depend on the level of postnatal maturity. 

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