What are some important factors (risks) to consider when evaluating a fetal heart rate
strip? - ANS --*PNLs* (abnormal?)
--weight gain/loss
--Maternal age
--*Gestational age*
--*MATERNAL vital signs*
--*Membrane status*
--*Cervical exam*
What are the easiest ways for assessment of maternal oxygenation status? - ANS
*Pulse Ox* (& other vital signs, RR)
*Blood gas* (if indicated, asthma exacerbation)
*Lung soungs* (pneumonia, pulmonary edema?)
What effect can *HTN/Preeclampsia* have on the Placenta? - ANS
*VASOCONSTRICTION*
which adversely effects placental perfusion and can lead to:
--*IUGR*
--*Infarcts* (decreases functional area of the placenta & functional capacity)
Placental Infarcts - ANS - Necrosis of placental villi
- Anechoic or Hypoechoic areas in placenta
Placental infarcts will do what to the placental function? - ANS *DECREASE functional
area* of placenta
*DECREASE functional capacity*
What effect can *Diabetes* have on Placental perfusion? - ANS Secondary to *Maternal
Vasculopathy* & HYPERglycemia* this can lead to:
*reduced utero-placental perfusion* = *IUGR*
What can change for fetal energy demands when you have a "DIABETIC mother"
uncontrolled and there is *Fetal HYPERglycemia & HYPERinsulinemia*? - ANS Fetal
hyperglycemia & hyperinsulinemia can cause:
*Increased fetal O2 consumption* which may induce *fetal hypoxemia & acidosis* if the
O2 needs of the fetus are not met by the placenta.
,What are some common conditions which could lead to a *POOR maternal Oxygenation
status*? - ANS Respiratory DEPRESSION (*Meds or Seizure*)
*Pulmonary EMBOLISM*
*Pneumonia*
*Asthma*
*Atelectasis*
ARDS
*Smoking*
*ANEMIA*
What are some examples of *collagen-vascular diseases*? HOw does these effect
pregnancy? - ANS *Rheumatoid arthritis*
*Scleroderma*
*SLE* (lupus)
= maternal *vasocontriction* which can lead to interruptions in placental & uterine blood
flow
--'IUGR'
What fetal cardiac condition may you see in a mother with *SLE* (systemic lupus
erythematosis)? - ANS *Secondary Heart BLOCK*
*Renal disease* (CKD, etc.) could cause what? - ANS *Maternal
VASOCONSTRICTION*
= maternal *vasocontriction* which can lead to interruptions in placental & uterine blood
flow
--'IUGR'
*Thyroid Disease* could cause what? - ANS *Maternal VASOCONSTRICTION*
= maternal *vasocontriction* which can lead to interruptions in placental & uterine blood
flow
--'IUGR'
What is the concern with *cardiac disease* in expectant mothers? - ANS Cardiac
disease ----> impaired cardiac function or even cardiac failure
---> *Decrease cardiac output* ----> decreased blood flow/oxygen flow through placenta
IUGR, etc.
,What are some common causes of *Maternal HYPOTENSION*? - ANS *Supine
hypotension* of pregnancy
*VASODILATION* 2/2 epidural
This will *DECREASE O2 & blood flow through the placenta*.
What are the *Maternal* 'EXTRINSIC factors' which effect delivery of bloos & availability
of blood/O2 through placenta? - ANS 1. *Maternal Oxygen status*
--fetus relies on the ability of mother to be well-oxygenated
Anything that interferes with maternal oxygenation has the potential to compromise the
fetus.
2. *Maternal HEMOGLOBIN levels* O2 is released from the maternal Hgb & attaches to
fetal Hgb (*O2 carrying capacity*)
3. *Cardiac OUTPUT* -- decreased CO affects blood flow to the uterus & placenta.
In terms of Maternal Oxygen Status, in order for there to be *adequate arterial oxygen
tension (PaO2)* -- there needs to be what? - ANS PaO2 = immediately available O2 for
exchange
What are the *'Placental factors'* which can effect the efficiency of *Uteroplacental
perfusion*? - ANS 1. '*UTERINE Blood flow*
2. Damaged chorionic vessels* (leaking into the intervillouos space)
3. *Decrease in SIZE or functioning area* of the *Placenta*
4. *Placental Reserve*
There can be Acute vs. Chronic decreases in uteroplacental function.
Describe *Uterine BLOOD flow* changes during pregnancy.
--rate, % of CO, % to placenta vs. uterus - ANS UTERINE BLOOD FLOW:
-Nonpregnancy rate is usually 50ml/min, during *pregnancy = 700ml/min*!!
-*10-15%* of total *cardiac output*
*70-90%* of this blood flow goes to *PLACENTA/intervillous space* = intervillous space
perfusion is dependent on adequate uterine blood flow.
, Compare Acute vs. Chronic changes in uteroplacental perfusion/function. - ANS
*ACUTE*:
sudden drop in placental function limits O2 & CO2 exchange which can lead to
*fetal asphyxia*
*CHRONIC*:
if there is a chronic decrease in placental function this may be more likely to limit
*carbohydrate transfer* & can lead to fetal growth restriction.
Due to high rate of uterin blood flow in pregnancy - what level of decrease can be
tolerated prior to severe effects on fetal status? - ANS Uterine blood flow can *decrease
by 50%* befoer SEVERE acidosis develops.
What are some common causes of *damage to the chorionic vessels* which causes
leakage of blood into the intervillous space (fetal-maternal hemorrhage)? - ANS
Damaged chorionic vessels:
*abdominal trauma*
*'spontaneous' placental abruption* (or secondary to cocaine, HTN disorders, etc)
*Invasive procedures* (amniocentesis, CVS)
*Ruptured vasa previa*
What are four main ways that the *size or functional area* of the *placenta* can be
compromised? - ANS 1. *ABRUPTION*: decreases the functional AREA of placenta
(spontaneous, trauma, procedures)
2. *MATERNAL DISEASE* (HTN)
-disease processes can cause smaller placenta
-smaller placenta decreases gas exchange results in FGR, asphyxia & malnourishment.
3. *INFECTION*
4. *CONGENITAL DEFECTS*
What is the *placental reserve*? - ANS *OXYGEN in the placenta DURING a
CONTRACTION* when there is *NO other blood flow entering the placenta*
This is the O2 reserve that continues oxygenating the fetus until the contraction ends!!!
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