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Relias - Fetal Heart Monitoring Questions and Answers Graded A+ 2024/2025
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Relias - Fetal Heart Monitoring Questions and Answers Graded A+ 2024/2025
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Relias - Fetal Heart MonitoringUterine blood deliver - ANS- uterine arteries deliver oxygenated blood to spiral arteries which
carry oxygen rich blood to intervillous area of placenta that has fetal capillaries
- fetal capillaries bring the O2 rich blood to umbilical VEIN that goes to fetus
-in contrast, the umbilical ARTERIES return waste merchandise to that intervillous space that
move into mother's venous gadget
Potential troubles that negatively affect fetal oxygenation - ANS*Maternal Oxygenation:*
bronchial asthma, hyper- or hypo- air flow
*Maternal Circulation:* decreased maternal cardiac output, hypotension, reduced Hgb
*Placental O2 and CO2 Exchange:* postterm, abruption, HTN, hypotension, uterine
tachysystole
*Fetal circulate:* cord compression or occlusion
Fetal hypoxemia - ANS- can arise d/t decreased fetal O2 reserves, immoderate uterine pastime,
or decreased uteroplacental blood drift
- worsening fetal hypoxemia can lead to bizarre FHR patterns, by and large minimal or absent
variability from acidemia
(1) hypoxemia vs. (2) hypoxia - ANS1 - reduce O2 in blood
2 - reduced O2 shipping at tissue stage
Fetal anaerobic metabolism - ANS- occurs when long term O2 transport is insufficient to meet
mobile needs of tissues
- effects in production of lactic acid and different noncarbonic acids
- ACIDOSIS is the presence of excessive acids in tissues
acidosis - ANSpH beneath 7.35
pH is low
(acidosis is the process that leads to low blood pH, or acidemia)
, alkalosis - ANSpH above 7.45
pH is excessive
buffers - ANS- help hold acid base homeostasis
- 2 main fetal buffers are plasma bicarbonate and hgb
base extra and base deficit - ANS- base deficit is expressed as a nice range
- base excess is expressed as a poor quantity
~ they may be equivalent and phrases are used interchangeably ~
fetal acidosis - ANS- while O2 is decreased to fetus, tissue hypoxia effects in acidosis, which
then suggests a drop in pH, a loss of bicarb, and boom in base deficit
acidemia - ANSassoc w/ considerable, deleterious effects on vital organ and body feature
fetal hypoxia for the duration of birth - ANSassoc w/ neonatal despair, low apgars, neonatal
encephalopathy, and cerebral palsy
respiratory acidosis - ANS*low pH (< 7.10), high pCO2 (> 60), normal base deficit ( < 12)*
- increase of pCO2 for fetus that lowers pH but does not have an effect on base deficit
elements that make contributions to resp acidosis - ANS- sudden decrease in placental or twine
perfusion
- uterine tachysystole
- maternal hypoventilation
metabolic acidosis - ANS*ph < 7.10 , everyday pCO2 (<60), high base deficit (>12)*
- a better base deficit (including > 12) has been assoc w/better threat for extreme neonatal
headaches
- most commonplace purpose of metabolic acidosis in fetus is r/t inadequate O2 shipping
- prolonged hypoxic insult to fetus consequences in depletion of bicarb, which is a base buffer
that normalizes pH stages
mixed acidosis - ANS*pH < 7.10 , high pCO2 > 60, and high base deficit >12*
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