Ms. Harmons focused review Flashcards
this is what harmon told us to focus on
Pulmonary changes in reference to inhalation agents
-MV is increased by 50% TV by 40% and RR by 10% the increased MV and decreased FRC => causes rapid increased alveolar concentrations of inhaled anesthestics basically gas uptake is faster!!!
uterine blood flow is up to how much mL/min
500-700 mL/min
Is the uterus autoregulated
no, it depends on the mothers BP
what causes decreases in uterine blood flow?
mothers hypotension
do epidurals or spinal anesthesia alter uterine blood flow?
not if maternal hypotension is avoided
what do contractions do to uterine blood flow?
Decreases it
An Anesthetic consideration is that which pressor is NOT associated with significant decreases in uterine blood flow?
Ephedrine
Placental exchange occurs primarily by what?
diffusion
1st stage Pain what type of pain? what causes the pain? what type of nerve fibers? where to the fibers origionate? pain characteristics?
-VISCERAL -caused by uterine contractions an ddilation of cervix -Autonomic C fibers -enter the dorsal horn of the spinal cord T10-L1 -dull- aching pain (how to remember For Jake) know the C visCeral pain caused by Contractions and dilation Cervix autonomic C fibers
2nd stage Pain what type of pain? what causes the pain? what type of nerve fibers? name of the nerves? where to the fibers origionate?
-SOMATIC -caused by the stretching of the vagina and perineum by desecent of the fetus -A-Delta -pudendal nerves -enter spinal cord at posterior roots S2-4 (how to remember Somatic Seecond stage remember the S)
what is the treatment for aspiration prophylaxis for all pregnant women? give doses and route!
Reglan 10mg IV Zantac 50mg IV Bicitra 30 mL PO
what is Beat to beat variability? Is it normal? what does it indicate?
FHR that varies 5-20 BPM yes (completly normal) nothing no worries
what is early decelerations? is it normal? what does it indicate?
-the slowing of the FHF that begins with the onset of uterine contraction -yep (no worries no problems) -nothing NOT indicative of fetal distress
what is a late deceleration is it normal? what does it indicate? what test is recomended?
-slowing of FHF that begins 10-30 seconds after the onset of uteine contractions. -nope never - fetal distress - fetal scalp pH
what are variable decelerations? they are generally characterized by what? thought to be caused by what? are the bad? how can you fix it?
- variable in magnitude, duration and time of onset - generally characterized by a steep descent of FHR -umbilical cord compression -unless prolonged, they are usually benign - changing maternal position (all caused by compression of the cord)
what is it and what are the 6 defining characteristics?
early decelerations have the following characteristics:
- Occur with each uterine contraction
- Start and end with the contraction
- Gradually decrease in rate and then end in a return to baseline
- Are uniform in appearance
- Are associated with a mild decrease in FHR (20 bpm or less)
- Are accompanied by a loss in beat-to-beat variability during the deceleration (Plaus 1112)
what is this and what are the 4 defining characteristics
variable decelerations have the following characteristics:
- Vary in appearance, duration, depth, and shape
- Demonstrate abrupt onset and recovery
- Maintain beat-to-beat variability with the deceleration
- Are classified as severe if the FHR decreases by 60 bpm, if the FHR decreases to less than 60 bpm, or if the decelerations last 60 seconds or longer (Plaus 1112)
what is this and what are it’s 7 defining characteristics
late decelerations have the following characteristics:
- Occur with each uterine contraction
- Start between 10 and 30 seconds after the uterine contraction
- Gradually decrease in rate and end in a return to baseline
- Are uniform in appearance
- Vary in depth according to the strength of the uterine contraction
- May or may not be accompanied by beat-to-beat variability
- Are classified as severe if the FHR decreases by more than 45 bpm
Late decelerations are probably caused by a problem in the uteroplacental interface that results in fetal hypoxia and acidosis. Any late deceleration is a reason for concern. Even small (Plaus 1112)
WHat is this
normal beat-to-beat and long-term variability with fetal heart rate (FHR) of 150 to 160 beats per minute (bpm). The distance between the heavy vertical lines represents 60 seconds. The lighter vertical lines are 10 seconds apart (Plaus 1110)
What is this?
Poor beat-to-beat and long-term variability. The fetal heart rate was measured with a scalp electrode. (Plaus)
Plaus, Nagelhout and. Nurse Anesthesia, 4th Edition. W.B. Saunders Company, 022009. .
are VAA’s teratogens? and why or why not?
yes (potentially)
b/c unethical to test in prego
LA, VAAs, induction agents, opioids, and MR are all safe for the fetus when?
in clicical circumstances
Name14 teratogenic drugs?
ACEi’s
ETOH
COCAINE
COUMADIN
androgens
antithyroid
chemo
Diethystibesterol
Lead
Lithium
Mercury
Phenytoin
Streptomycin
Thalidomide
Trimethadione
Valproic acid
Pregnancy cat A
no risk identified in well controlled studies
Pregnancy Cat B
no adequate and well controlled studies in PREGNANT WOMEN, however animal studies have revealed no fetus harm
Pregnancy Cat C
no adequate and well controlled studies in PREGNANT WOMEN, however an adverse effect has been shown in animals
or
Adequate and well controlled studies in PREGNANT WOMENhave failed to show a risk to the fetus; but an adverse effect has been shown in an animal
Pregnancy Cat D
a risk to the fetus has been demonstrated in adequate, well controlled or observational studies in pregnant women; however the benefits of therapy may outweigh the potential risk
Pregnancy cat X
positive evidence of fetal abnormalities has been demonstrated in adequate well controlled studies or observational studies in pregnant woman or animals, the drug is contraindicated in women who are or may became pregnant
what teratogenic effect do benzo’s cause
cleft anomalies
what teratogenic effects does cocain how
vasoconstriction
hypoxia
abruption
what teratogenis effects do halogenated inhalation drugs have
in animal studies after 8-12 hours of exposure during organogenesis( effects were seen)
what teratogenic effects do NSAIDs have
constrict or close ductus arteriosis (usually avoided)
complications of tocylitics
pulm edema
arrythmias
hypokalemia
what is present when the placenta implants in advance of the fetal presenting part?
Placenta previa
3 types of placenta previa? and what are they?
total
partial
marginal
what is marginal placenta previa?
placenta just reaches the internal OS but does not cover it AKA (low-lying)
what is partial placenta previa?
placenta partially covers the internal OS
what is complete placenta previa?
placenta completely covers internal OS
what can cause placenta previa?
multiparity
advanced maternal age
previous C-section (or uterine sx)
Previous placental previa
*****************************
what is the classic presentation of placentia previa
PAINLESS vaginal bleeding during the second or third trimester
what is defined as separation of placenta from the decidua basilis (endometrium) before delivery of fetus?
Placental abruption
look at all 3 and see differences
what are associated factors with placental abruption
HTN
advanced age and parity
tobacco use
COCAINE
trauma
PROM
Hx of placental abruption
what is a uterine wall defect resulting in fetal distress and/ or maternal hemmorrhage sufficient enough to require a C-section or post partum laparotomy?
uterine rupture
where does uterine rupture usually occur?
classic rupture of uterine scar
what is the prefered definative approach to uterine rupture?
hysterectomy
postpartum hemorrhage is defined as what?
> 300 ml after delivery
(or a 10% decrease in HCT from admission to portpartum period)
what is primary postpartum hemorrhage
occurs during first 24 hrs after delivery
what is 2ndary postpartum hemorrhage
occurs b/t 24 hrs and 6 wks postpartum
what are 3 abnormal placental implantations
Accreta- adherance to myometrium no invasion or passage to muscle
Increata- invasion on myometrium
Percreta- invasion of uterine serosa or other pelvic structures
5 categories of tocolytics and names and SE if known
Beta receptor agonist (terbutaline, ritodine) s/e of tachycardia
Magnesium sulfate (Ca++ antagonist)
CCB (procardia, Nifidipine)
Prostaglandin sysnthesis inhibitors (ASA, NSAIDs, Indomethacin) s/e ductus arterious closure
Oxytocin antagonist
MAgnesium sulfate
- used for what 2 things?
- causes relaxation of ______, ________, and ________ smooth muscle
- Alters _______ transport and availability
- normal serum levels are ____ - _____ mg/dL
- therapeutic serum level is _____-____ mg/dL
- tocolysis and PIH
- vascular, bronchial, and uterine
- calcium
- 1.8-3
- 4-8
Magnesium s/e
- DTR loss at _____ mEq/L
- Cardiac arrest at ______ mEq/L
- think of it as a partial _________ ___________
- rapidly removed from the body, can be antagonized with _______ ___________
- side effect s/s
- 10
- 25
- neiromuscular blockade
- calcium chloride (3x’s more Ca++ than glucanate)
- muscle weakness/ loss of DTR/ head ache/ dizziness/ nausea/ respi changes/ ECG changes/ flushing
what is important to remamber about magnesiums s/e
it crosses the placenta so all s/e mom gets baby gets also
s/s of PIH (preeclampsia)?
HTN
edema
proteinuria
h/a
visual disturbances
confusion
RUQ pain
Epigastric pain
Oligohydroaminious
impaired renal fxn
oliguria <500 ml/day
pulm edema
anemia
thrombocytopenia <100,000
fetal inpired liver fxn
Diagnosis of PIH preeclamsia is based on what?
sustained BP > 140/90
2+ or 300 mg/24hr proteinuria
pretibial edema
what is used to control PIH
magnesium
preeclampsia anesthesia preference
regional (as long as plt is ok)
can decrease BP
what are predisposing factors to PIH/preeclampsia
highest is primigravidas <20 y/o
and older the 35
what about esmolol use in PIH/ preeclampsia
held great promise, but found to be a BAD idea
crosses the placenta and causes a clinically significant feta beta blockade
BABY WILL COME OUT WITH ASYSTOLE
est blood loss for vaginal birth
approx 500ml
est blood loss for c-section
700 for c-section (somewhere she said 1500 was ok)
CV compensatory response to aortocaval compression
decreased venous return = decreased SV and CO
response is
tachycardia
casoconstriction of lower extremities
G2P2002
G# of pregnancies
P # of kids
F P and L (full term, preterm, abortion, living)
2 pregnancies
2 full term
0 preterm
0 abortions
2 living
G1P0000
1 pregnancy
0 fullterm
0 preterm
0 abortion
0 living
(this is her first pregnancy)
severe preeclampsia is said to exist when what conditions are present?
Bp > 160/110
3+ or 4+ proteinuria
UOP < 20 ml/hr
CNS signs (blurred vision, changes in metation)
Pulm edema
epigastric pain
